2021/07/12 更新

写真a

オウ ヒデマサ
王 英正
OH Hidemasa
所属
岡山大学病院 教授
職名
教授
外部リンク

学位

  • 医学博士 ( 大阪大学 )

研究キーワード

  • 再生医学

  • 細胞療法

  • 心不全

  • 心筋細胞

  • 幹細胞

  • Cell Therapy

  • Cardiac Regeneration

  • Stem Cells

研究分野

  • ライフサイエンス / 循環器内科学

経歴

  • - Professor,University Hospital of Medicine and Dentistry,Okayama University

    2010年

      詳細を見る

  • - 岡山大学岡山大学病院 教授

    2010年

      詳細を見る

  • Associate Professor,University Hospital of Medicine and Dentistry,Okayama University

    2009年 - 2010年

      詳細を見る

  • 岡山大学岡山大学病院 准教授   Okayama University Hospital

    2009年 - 2010年

      詳細を見る

  • Associate Professor

    2008年 - 2009年

      詳細を見る

  • 京都府立医科大学

    2008年 - 2009年

      詳細を見る

  • 京都大学付属病院 准教授

    2003年 - 2008年

      詳細を見る

  • Associate Professor

    2003年 - 2008年

      詳細を見る

▼全件表示

 

MISC

  • Impact of cardiac progenitor cells on heart failure and survival in single ventricle congenital heart disease.

    Sano T, Ousaka D, Goto T, Ishigami S, Hirai K, Kasahara S, Ohtsuki S, Sano S, Oh H

    Circulation Research   122 ( 7 )   994 - 1005   2018年

  • Impact of cardiac progenitor cells on heart failure and survival in single ventricle congenital heart disease.

    Sano T, Ousaka D, Goto T, Ishigami S, Hirai K, Kasahara S, Ohtsuki S, Sano S, Oh H

    Circulation Research   122 ( 7 )   994 - 1005   2018年

  • Cell Therapy Trials in Congenital Heart Disease

    Hidemasa Oh

    CIRCULATION RESEARCH   120 ( 8 )   1353 - 1366   2017年4月

     詳細を見る

    記述言語:英語   掲載種別:書評論文,書評,文献紹介等   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Dramatic evolution in medical and catheter interventions and complex surgeries to treat children with congenital heart disease (CHD) has led to a growing number of patients with a multitude of long-term complications associated with morbidity and mortality. Heart failure in patients with hypoplastic left heart syndrome predicated by functional single ventricle lesions is associated with an increase in CHD prevalence and remains a significant challenge. Pathophysiological mechanisms contributing to the progression of CHD, including single ventricle lesions and dilated cardiomyopathy, and adult heart disease may inevitably differ. Although therapeutic options for advanced cardiac failure are restricted to heart transplantation or mechanical circulatory support, there is a strong impetus to develop novel therapeutic strategies. As lower vertebrates, such as the newt and zebrafish, have a remarkable ability to replace lost cardiac tissue, this intrinsic self-repair machinery at the early postnatal stage in mice was confirmed by partial ventricular resection. Although the underlying mechanistic insights might differ among the species, mammalian heart regeneration occurs even in humans, with the highest degree occurring in early childhood and gradually declining with age in adulthood, suggesting the advantage of stem cell therapy to ameliorate ventricular dysfunction in patients with CHD. Although effective clinical translation by a variety of stem cells in adult heart disease remains inconclusive with respect to the improvement of cardiac function, case reports and clinical trials based on stem cell therapies in patients with CHD may be invaluable for the next stage of therapeutic development. Dissecting the differential mechanisms underlying progressive ventricular dysfunction in children and adults may lead us to identify a novel regenerative therapy. Future regenerative technologies to treat patients with CHD are exciting prospects for heart regeneration in general practice.

    DOI: 10.1161/CIRCRESAHA.117.309697

    Web of Science

    researchmap

  • Intracoronary Cardiac Progenitor Cells in Single Ventricle Physiology: The PERSEUS Randomized Phase 2 Trial.

    Ishigami S, Ohtsuki S, Eitoku T, Ousaka D, Kondo M, Kurita Y, Hirai K, Fukushima Y, Baba K, Goto T, Horio N, Kobayashi J, Kuroko Y, Kotani Y, Arai S, Iwasaki T, Sato S, Kasahara S, Sano S, Oh H

    Circulation Research   120 ( 7 )   1162 - 1173   2017年

     詳細を見る

  • 体性幹細胞を用いた心臓再生医療の最前線

    石神修大, 大月審一, 笠原真悟, 佐野俊二, 王 英正

    臨床医薬   33 ( 4 )   125 - 132   2017年

     詳細を見る

  • Cell Therapy Trials in Congenital Heart Disease

    H. Oh

    Circulation Research   120 ( 8 )   1353 - 1366   2017年

  • Transcoronary cell infusion with the stop-flow technique in children with single-ventricle physiology.

    Eitoku T, Baba K, Kondou M, Kurita Y, Fukushima Y, Hirai K, Ohtsuki S, Ishigami S, Sano S, Oh H

    Pediatric Intervention   60 ( 3 )   240 - 246   2017年

     詳細を見る

  • 先天性心疾患に対する心筋再生医療

    石神修大, 大月審一, 笠原真悟, 佐野俊二, 王 英正

    Heart View   5 ( 5 )   547 - 551   2017年

     詳細を見る

  • Cell Therapy Trials in Congenital Heart Disease

    Oh H

    Circulation Research   120 ( 8 )   1353 - 1366   2017年

  • Transcoronary cell infusion with the stop-flow technique in children with single-ventricle physiology.

    Eitoku T, Baba K, Kondou M, Kurita Y, Fukushima Y, Hirai K, Ohtsuki S, Ishigami S, Sano S, Oh H

    Pediatric Intervention   60 ( 3 )   240 - 246   2017年

     詳細を見る

  • 心臓内幹細胞による心不全疾患の治療

    佐野俊和, 大月審一, 佐野俊二, 王 英正

    BIO Clinica   31 ( 10 )   29 - 33   2016年

     詳細を見る

  • 心臓内幹細胞を用いた心臓再生医療

    平井健太, 大月審一, 佐野俊二, 王 英正

    心臓   48 ( 12 )   1334 - 1339   2016年

     詳細を見る

  • Challenges to success in heart failure: Cardiac cell therapy to treat patients with heart disease.

    Journal of Cardiology   2016年

  • Challenges to success in heart failure: Cardiac cell therapy to treat patients with heart disease.

    Hidemasa Oh, Hiroshi Ito, Shunji Sano

    Journal of Cardiology   2016年

  • Intracoronary Autologous Cardiac Progenitor Cell Transfer in Patients With Hypoplastic Left Heart Syndrome The TICAP Prospective Phase 1 Controlled Trial

    Shuta Ishigami, Shinichi Ohtsuki, Suguru Tarui, Daiki Ousaka, Takahiro Eitoku, Maiko Kondo, Michihiro Okuyama, Junko Kobayashi, Kenji Baba, Sadahiko Arai, Takuya Kawabata, Ko Yoshizumi, Atsushi Tateishi, Yosuke Kuroko, Tatsuo Iwasaki, Shuhei Sato, Shingo Kasahara, Shunji Sano, Hidemasa Oh

    CIRCULATION RESEARCH   116 ( 4 )   653 - 664   2015年2月

     詳細を見る

    記述言語:英語   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Rationale: Hypoplastic left heart syndrome (HLHS) remains a lethal congenital cardiac defect. Recent studies have suggested that intracoronary administration of autologous cardiosphere-derived cells (CDCs) may improve ventricular function.
    Objective: The aim of this study was to test whether intracoronary delivery of CDCs is feasible and safe in patients with hypoplastic left heart syndrome.
    Methods and Results: Between January 5, 2011, and January 16, 2012, 14 patients (1.8 +/- 1.5 years) were prospectively assigned to receive intracoronary infusion of autologous CDCs 33.4 +/- 8.1 days after staged procedures (n=7), followed by 7 controls with standard palliation alone. The primary end point was to assess the safety, and the secondary end point included the preliminary efficacy to verify the right ventricular ejection fraction improvements between baseline and 3 months. Manufacturing and intracoronary delivery of CDCs were feasible, and no serious adverse events were reported within the 18-month follow-up. Patients treated with CDCs showed right ventricular ejection fraction improvement from baseline to 3-month follow-up (46.9%+/- 4.6% to 52.1%+/- 2.4%; P=0.008). Compared with controls at 18 months, cardiac MRI analysis of CDC-treated patients showed a higher right ventricular ejection fraction (31.5%+/- 6.8% versus 40.4%+/- 7.6%; P=0.049), improved somatic growth (P=0.0005), reduced heart failure status (P=0.003), and lower incidence of coil occlusion for collaterals (P=0.007).
    Conclusions: Intracoronary infusion of autologous CDCs seems to be feasible and safe in children with hypoplastic left heart syndrome after staged surgery. Large phase 2 trials are warranted to examine the potential effects of cardiac function improvements and the long-term benefits of clinical outcomes.

    DOI: 10.1161/CIRCRESAHA.116.304671

    Web of Science

    researchmap

  • Epigenetic modification in congenital heart diseases by using stem cell technologies

    Kobayashi J, Sano S, Oh H

    Stem Cell Epigenetics   1 ( 2 )   e550   2015年

     詳細を見る

  • Cardiac stem cell therapies for congenital heart diseases

    Ishigami S, Sano S, Oh H

    Stem Cell and Translational Investigation   1 ( 2 )   e800   2015年

     詳細を見る

  • 小児心不全に対する心臓内幹細胞自家移植療法

    日本小児血液・がん学会誌   52 ( 3 )   2015年

     詳細を見る

  • 疾患特異的iPS細胞を用いた先天性心疾患の病態解明

    小児循環器学会雑誌   2015年

     詳細を見る

  • Transcoronary infusion of cardiac progenitor cells in hypoplastic left heart syndrome: Three-year follow-up of the Transcoronary Infusion of Cardiac Progenitor Cells in Patients With Single-Ventricle Physiology (TICAP) trial.

    Tarui S, Ishigami S, Ousaka D, Kasahara S, Ohtsuki S, Sano S, Oh H

    J Thorac Cardiovasc Surg.   150 ( 5 )   1198 - 1208   2015年

  • Directed Differentiation of Patient-Specific Induced Pluripotent Stem Cells Identifies the Transcriptional Repression and Epigenetic Modification of NKX2-5, HAND1, and NOTCH1 in Hypoplastic Left Heart Syndrome

    Junko Kobayashi, Masashi Yoshida, Suguru Tarui, Masataka Hirata, Yusuke Nagai, Shingo Kasahara, Keiji Naruse, Hiroshi Ito, Shunji Sano, Hidemasa Oh

    PLOS ONE   9 ( 7 )   e102796-e102796   2014年7月

     詳細を見る

    記述言語:英語   出版者・発行元:PUBLIC LIBRARY SCIENCE  

    The genetic basis of hypoplastic left heart syndrome (HLHS) remains unknown, and the lack of animal models to reconstitute the cardiac maldevelopment has hampered the study of this disease. This study investigated the altered control of transcriptional and epigenetic programs that may affect the development of HLHS by using disease-specific induced pluripotent stem (iPS) cells. Cardiac progenitor cells (CPCs) were isolated from patients with congenital heart diseases to generate patient-specific iPS cells. Comparative gene expression analysis of HLHS-and biventricle (BV) heart-derived iPS cells was performed to dissect the complex genetic circuits that may promote the disease phenotype. Both HLHS-and BV heart-derived CPCs were reprogrammed to generate disease-specific iPS cells, which showed characteristic human embryonic stem cell signatures, expressed pluripotency markers, and could give rise to cardiomyocytes. However, HLHS-iPS cells exhibited lower cardiomyogenic differentiation potential than BV-iPS cells. Quantitative gene expression analysis demonstrated that HLHS-derived iPS cells showed transcriptional repression of NKX2-5, reduced levels of TBX2 and NOTCH/HEY signaling, and inhibited HAND1/2 transcripts compared with control cells. Although both HLHS-derived CPCs and iPS cells showed reduced SRE and TNNT2 transcriptional activation compared with BV-derived cells, co-transfection of NKX2-5, HAND1, and NOTCH1 into HLHS-derived cells resulted in synergistic restoration of these promoters activation. Notably, gain- and loss-of-function studies revealed that NKX2-5 had a predominant impact on NPPA transcriptional activation. Moreover, differentiated HLHS-derived iPS cells showed reduced H3K4 dimethylation as well as histone H3 acetylation but increased H3K27 trimethylation to inhibit transcriptional activation on the NKX2-5 promoter. These findings suggest that patient-specific iPS cells may provide molecular insights into complex transcriptional and epigenetic mechanisms, at least in part, through combinatorial expression of NKX2-5, HAND1, and NOTCH1 that coordinately contribute to cardiac malformations in HLHS.

    DOI: 10.1371/journal.pone.0102796

    Web of Science

    researchmap

  • MURC/Cavin-4 facilitates recruitment of ERK to caveolae and concentric cardiac hypertrophy induced by α1-adrenergic receptors.

    Ogata T, Naito D, Nakanishi N, Hayashi YK, Taniguchi T, Miyagawa K, Hamaoka T, Maruyama N, Matoba S, Ikeda K, Yamada H, Oh H, Ueyama T

    Proc Natl Acad Sci U S A.   111 ( 10 )   3811 - 3816   2014年3月

     詳細を見る

  • Stem cell therapies in patients with single ventricle physiology.

    Methodist Debakey Cardiovascular Journal.   10 ( 2 )   77 - 81   2014年

     詳細を見る

  • 小児心不全の再生医療からのアプローチ

    石神修大, 佐野俊二, 王 英正

    移植   50 ( 6 )   54 - 63   2014年

     詳細を見る

  • 先天性心疾患外科手術における再生医療

    循環器内科   75 ( 1 )   87 - 93   2014年

     詳細を見る

  • 心筋幹細胞を用いた先天性心疾患に対する心筋再生医療

    樽井俊, 佐野俊二, 王 英正

    月刊循環器   3 ( 9 )   69 - 76   2013年

     詳細を見る

  • 先天性心疾患に対する心筋再生医療

    小林純子, 佐野俊二, 王 英正

    循環器内科   71 ( 4 )   360 - 368   2012年

     詳細を見る

  • 小児心不全への細胞治療の現状と展望

    王 英正

    呼吸と循環   60   S1-S4   2012年

     詳細を見る

  • 先天性心疾患に対する心筋再生医療

    小林純子, 佐野俊二, 王 英正

    循環器内科   71   360 - 368   2012年

     詳細を見る

  • テロメア生物学から心筋再生医療の実用化へ

    王 英正

    岡山医学会雑誌   124   27 - 34   2012年

     詳細を見る

  • Molecular Genetic and Functional Characterization Implicate Muscle-Restricted Coiled-Coil Gene (MURC) as a Causal Gene for Familial Dilated Cardiomyopathy

    Gabriela Rodriguez, Tomomi Ueyama, Takehiro Ogata, Grazyna Czernuszewicz, Yanli Tan, Gerald W. Dorn, Roberta Bogaev, Katsuya Amano, Hidemasa Oh, Hiroaki Matsubara, James T. Willerson, Ali J. Marian

    CIRCULATION-CARDIOVASCULAR GENETICS   4 ( 4 )   349 - U47   2011年8月

     詳細を見る

    記述言語:英語   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Background-Dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM) are classic forms of systolic and diastolic heart failure, respectively. Mutations in genes encoding sarcomere and cytoskeletal proteins are major causes of HCM and DCM. MURC, encoding muscle-restricted coiled-coil, a Z-line protein, regulates cardiac function in mice. We investigated potential causal role of MURC in human cardiomyopathies.
    Methods and Results-We sequenced MURC in 1199 individuals, including 383 probands with DCM, 307 with HCM, and 509 healthy control subjects. We found 6 heterozygous DCM-specific missense variants (p.N128K, p.R140W, p.L153P, p.S307T, p.P324L, and p.S364L) in 8 unrelated probands. Variants p.N128K and p. S307T segregated with inheritance of DCM in small families (chi(2) = 8.5, P=0.003). Variants p.N128K, p.R140W, p.L153P, and p.S364L were considered probably or possibly damaging. Variant p.P324L recurred in 3 independent probands, including 1 proband with a TPM1 mutation (p.M245T). A deletion variant (p.L232-R238del) was present in 3 unrelated HCM probands, but it did not segregate with HCM in a family who also had a MYH7 mutation (p.L907V). The phenotype in mutation carriers was notable for progressive heart failure leading to heart transplantation in 4 patients, conduction defects, and atrial arrhythmias. Expression of mutant MURC proteins in neonatal rat cardiac myocytes transduced with recombinant adenoviruses was associated with reduced RhoA activity, lower mRNA levels of hypertrophic markers and smaller myocyte size as compared with wild-type MURC.
    Conclusions-MURC mutations impart loss-of-function effects on MURC functions and probably are causal variants in human DCM. The causal role of a deletion mutation in HCM is uncertain. (Circ Cardiovasc Genet. 2011;4:349-358.)

    DOI: 10.1161/CIRCGENETICS.111.959866

    Web of Science

    researchmap

  • Molecular Genetic and Functional Characterization Implicate Muscle-Restricted Coiled-Coil Gene (MURC) as a Causal Gene for Familial Dilated Cardiomyopathy

    Gabriela Rodriguez, Tomomi Ueyama, Takehiro Ogata, Grazyna Czernuszewicz, Yanli Tan, Gerald W. Dorn, Roberta Bogaev, Katsuya Amano, Hidemasa Oh, Hiroaki Matsubara, James T. Willerson, Ali J. Marian

    CIRCULATION-CARDIOVASCULAR GENETICS   4 ( 4 )   349 - U47   2011年8月

     詳細を見る

    記述言語:英語   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Background-Dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM) are classic forms of systolic and diastolic heart failure, respectively. Mutations in genes encoding sarcomere and cytoskeletal proteins are major causes of HCM and DCM. MURC, encoding muscle-restricted coiled-coil, a Z-line protein, regulates cardiac function in mice. We investigated potential causal role of MURC in human cardiomyopathies.
    Methods and Results-We sequenced MURC in 1199 individuals, including 383 probands with DCM, 307 with HCM, and 509 healthy control subjects. We found 6 heterozygous DCM-specific missense variants (p.N128K, p.R140W, p.L153P, p.S307T, p.P324L, and p.S364L) in 8 unrelated probands. Variants p.N128K and p. S307T segregated with inheritance of DCM in small families (chi(2) = 8.5, P=0.003). Variants p.N128K, p.R140W, p.L153P, and p.S364L were considered probably or possibly damaging. Variant p.P324L recurred in 3 independent probands, including 1 proband with a TPM1 mutation (p.M245T). A deletion variant (p.L232-R238del) was present in 3 unrelated HCM probands, but it did not segregate with HCM in a family who also had a MYH7 mutation (p.L907V). The phenotype in mutation carriers was notable for progressive heart failure leading to heart transplantation in 4 patients, conduction defects, and atrial arrhythmias. Expression of mutant MURC proteins in neonatal rat cardiac myocytes transduced with recombinant adenoviruses was associated with reduced RhoA activity, lower mRNA levels of hypertrophic markers and smaller myocyte size as compared with wild-type MURC.
    Conclusions-MURC mutations impart loss-of-function effects on MURC functions and probably are causal variants in human DCM. The causal role of a deletion mutation in HCM is uncertain. (Circ Cardiovasc Genet. 2011;4:349-358.)

    DOI: 10.1161/CIRCGENETICS.111.959866

    Web of Science

    researchmap

  • 小児心不全への細胞治療

    樽井 俊, 佐野俊二, 王 英正

    Medical Science Digest   37   439 - 442   2011年

     詳細を見る

  • PARM-1 is an Endoplasmic Reticulum Molecule Involved in Endoplasmic Reticulum Stress-induced Apoptosis in Rat Cardiac Myocytes.

    Isodono K, Takahashi T, Imoto H, Nakanishi N, Ogata T, Asada S, Adachi A, Ueyama T, Oh H, Matsubara H

    PLos ONE   18 ( 5 )   e9746-e9746   2010年

  • Stem Cell Engineering for Cardiac Tissue Regeneration

    Masashi Yoshida, Hidemasa Oh

    CARDIOLOGY   115 ( 3 )   191 - 193   2010年

     詳細を見る

    記述言語:英語   出版者・発行元:KARGER  

    DOI: 10.1159/000281839

    Web of Science

    researchmap

  • Stem Cell Engineering for Cardiac Tissue Regeneration

    Masashi Yoshida, Hidemasa Oh

    CARDIOLOGY   115 ( 3 )   191 - 193   2010年

     詳細を見る

    記述言語:英語   出版者・発行元:KARGER  

    DOI: 10.1159/000281839

    Web of Science

    researchmap

  • Deficiency of Nectin-2 Leads to Cardiac Fibrosis and Dysfunction Under Chronic Pressure Overload

    Seimi Satomi-Kobayashi, Tomomi Ueyama, Steffen Mueller, Ryuji Toh, Tomoya Masano, Tsuyoshi Sakoda, Yoshiyuki Rikitake, Jun Miyoshi, Hiroaki Matsubara, Hidemasa Oh, Seinosuke Kawashima, Ken-ichi Hirata, Yoshimi Takai

    HYPERTENSION   54 ( 4 )   825 - U268   2009年10月

     詳細を見る

    記述言語:英語   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    The intercalated disc, a cell-cell contact site between neighboring cardiac myocytes, plays an important role in maintaining the homeostasis of the heart by transmitting electric and mechanical signals. Changes in the architecture of the intercalated disc have been observed in dilated cardiomyopathy. Among cell-cell junctions in the intercalated disc, adherens junctions are involved in anchoring myofibrils and transmitting force. Nectins are Ca(2+)-independent, immunoglobulin-like cell-cell adhesion molecules that exist in adherens junctions. However, the role of nectins in cardiac homeostasis and integrity of the intercalated disc are unknown. Among the isoforms of nectins, nectin-2 and -4 were expressed at the intercalated disc in the heart. Nectin-2-knockout mice showed normal cardiac structure and function under physiological conditions. Four weeks after banding of the ascending aorta, cardiac function was significantly impaired in nectin-2-knockout mice compared with wild-type mice, although both nectin-2-knockout and wild-type mice developed similar degrees of cardiac hypertrophy. Banded nectin-2-knockout mice displayed cardiac fibrosis more evidently than banded wild-type mice. The disruption of the intercalated discs and disorganized myofibrils were observed in banded nectin-2-knockout mice. Furthermore, the number of apoptotic cardiac myocytes was increased in banded nectin-2-knockout mice. In the hearts of banded nectin-2-knockout mice, Akt remained at lower phosphorylation levels until 2 weeks after banding, whereas c-Jun N-terminal kinase and p38 mitogen-activated protein kinase were highly phosphorylated compared with those of wild-type mice. These results indicate that nectin-2 is required to maintain structure and function of the intercalated disc and protects the heart from pressure-overload induced cardiac dysfunction. (Hypertension. 2009; 54: 825-831.)

    DOI: 10.1161/HYPERTENSIONAHA.109.130443

    Web of Science

    researchmap

  • Cardiosphereを用いた心筋再生医療

    中西直彦, 竹原有史, 中岡幹彦, 赤壁佳樹, 王 英正, 松原弘明

    総合臨床   2009年

     詳細を見る

  • ヒト心臓由来幹細胞を用いた心不全への再生医療

    小出正洋, 星野 温, 山口真一郎, 岸田 聡, 竹原有史, 王 英正, 松原弘明

    再生誘導治療   2009年

     詳細を見る

  • 心筋幹細胞

    王 英正

    循環器科 特集   2009年

     詳細を見る

  • 重症心不全に対する細胞治療法

    竹原有史, 塘 義明, 天野克也, 王 英正, 長谷部直幸, 松原弘明

    循環器科 特集   2009年

     詳細を見る

  • Cardiosphereを用いた心筋再生医療

    中岡幹彦, 竹原有史, 中西直彦, 赤壁佳樹, 王 英正, 松原弘明

    再生医療   2009年

     詳細を見る

  • 自己心臓幹細胞を用いた心不全への細胞治療

    岸田 聡, 竹原有史, 王 英正, 松原弘明

    重症心不全の予防と治療   2009年

     詳細を見る

  • 新しい心臓再生法

    王 英正

    Medical View Point   2009年

     詳細を見る

  • Cardiosphereによる心筋再生

    竹原有史, 服部玲治, 松原弘明, 王 英正

    Annual Review 循環器   2009年

     詳細を見る

  • Cardiosphereによる心筋再生医療

    山口真一郎, 竹原有史, 天野克也, 高橋知三郎, 王 英正, 松原弘明

    分子心血管病 特集   2009年

     詳細を見る

  • Controlled Delivery of Basic Fibroblast Growth Factor Promotes Human Cardiosphere-Derived Cell Engraftment to Enhance Cardiac Repair for Chronic Myocardial Infarction

    Naofumi Takehara, Yoshiaki Tsutsumi, Kento Tateishi, Takehiro Ogata, Hideo Tanaka, Tomomi Ueyama, Tomosaburo Takahashi, Tetsuro Takamatsu, Masanori Fukushima, Masashi Komeda, Masaaki Yamagishi, Hitoshi Yaku, Yasuhiko Tabata, Hiroaki Matsubara, Hidemasa Oh

    JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY   52 ( 23 )   1858 - 1865   2008年12月

     詳細を見る

    記述言語:英語   出版者・発行元:ELSEVIER SCIENCE INC  

    Objectives This study was designed to determine whether controlled release of basic fibroblast growth factor ( bFGF) might improve human cardiosphere-derived cell (hCDC) therapy in a pig model of chronic myocardial infarction.
    Background Current cell therapies for cardiac repair are limited by loss of the transplanted cells and poor differentiation.
    Methods We conducted 2 randomized, placebo-controlled studies in immunosuppressed pigs with anterior myocardial infarctions. Four weeks after coronary reperfusion, 14 pigs were randomly assigned to receive an intramyocardial injection of placebo medium with or without bFGF-incorporating hydrogel implantation. As a second study, 26 pigs were randomized to receive controlled release of bFGF combined with or without hCDCs or bone marrow-derived mesenchymal stem cell transplantation 4 weeks after reperfusion.
    Results Controlled release of bFGF in ischemic myocardium significantly augmented the formation of microvascular networks to enhance myocardial perfusion and contractile function. When combined with cell transplantation, the additive effects of bFGF were confined to hCDC-injected animals, but were not observed in animals receiving human bone marrow-derived mesenchymal stem cell transplantation. This was shown by increased donor-cell engraftment and enhanced cardiomyocyte differentiation in the transplanted hearts, resulting in synergistically improved ventricular function and regional wall motion and reduced infarct size.
    Conclusions Controlled delivery of bFGF modulates the post-ischemic microenvironment to enhance hCDC engraftment and differentiation. This novel strategy demonstrates significant functional improvements after myocardial infarction and may potentially represent a therapeutic approach to be studied in a clinical trial in human heart failure. (J Am Coll Cardiol 2008; 52: 1858-65) (c) 2008 by the American College of Cardiology Foundation

    DOI: 10.1016/j.jacc.2008.06.052

    Web of Science

    researchmap

  • Stemming heart failure with cardiac- or reprogrammed-stem cells

    Kento Tateishi, Naofumi Takehara, Hiroaki Matsubara, Hidemasa Oh

    JOURNAL OF CELLULAR AND MOLECULAR MEDICINE   12 ( 6A )   2217 - 2232   2008年12月

     詳細を見る

    記述言語:英語   掲載種別:書評論文,書評,文献紹介等   出版者・発行元:WILEY-BLACKWELL  

    Despite extensive efforts to control myocyte growth by genetic targeting of the cell cycle machinery and small molecules for cardiac repair, adult myocytes themselves appeared to divide a limited number of times in response to a variety of cardiac muscle stresses. Rare tissue-resident stem cells are thought to exist in many adult organs that are capable of self-renewal and differentiation and possess a range of actions that are potentially therapeutic. Recent studies suggest that a population of cardiac stem cells (CSCs) is maintained after cardiac development in the adult heart in mammals including human beings; however, homeostatic cardiomyocyte replacement might be stem cell-dependent, and functional myocardial regeneration after cardiac muscle damage is not yet considered as sufficient to fully maintain or reconstitute the cardiovascular system and function. Although it is clear that adult CSCs have limitations in their capabilities to proliferate extensively and differentiate in response to injury in vivo for replenishing mature car-diomyocytes and potentially function as resident stem cells. Transplantation of CSCs expanded ex vivo seems to require an integrated strategy of cell growth-enhancing factor(s) and tissue engineering technologies to support the donor cell survival and subsequent proliferation and differentiation in the host microenvironment. There has been substantial interest regarding the evidence that mammalian fibroblasts can be genetically reprogrammed to induced pluripotent stem (iPS) cells, which closely resemble embryonic stem (ES) cell properties capable of differentiating into functional cardiomyocytes, and these cells may provide an alternative cell source for generating patient-specific CSCs for therapeutic applications.

    DOI: 10.1111/j.1582-4934.2008.00487.x

    Web of Science

    researchmap

  • Crossveinless-2 controls bone morphogenetic protein signaling during early cardiomyocyte differentiation in P19 cells

    Koichiro Harada, Akiko Ogai, Tomosaburo Takahashi, Masafumi Kitakaze, Hiroaki Matsubara, Hidemasa Oh

    JOURNAL OF BIOLOGICAL CHEMISTRY   283 ( 39 )   26705 - 26713   2008年9月

     詳細を見る

    記述言語:英語   出版者・発行元:AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

    Increasing evidence indicates that bone morphogenetic proteins (BMPs) are crucial for cardiac induction, specification, and development. Although signaling of BMPs is tightly regulated through soluble BMP-binding proteins, how they regulate BMP signaling during cardiac differentiation remains unknown. To identify molecules responsible for BMP signaling during early cardiomyocyte differentiation of P19 cells, cDNA subtraction was performed. We found a bimodal expression of the BMP-binding protein Crossveinless-2 (Cv2) during cardiomyocyte differentiation; Cv2 is temporally expressed earlier than cardiac transcription factors such as Nkx2.5 and Tbx5 and acts as a suppressor for BMP signaling in P19 cells. We established a P19 clonal cell line harboring a cardiac alpha-myosin heavy chain promoter-driven enhanced green fluorescent protein gene to monitor cardiac differentiation by flow cytometry. Treatment with BMP2 during the first 2 days of differentiation suppressed cardiomyocyte differentiation through activation of downstream targets Smad1/5/8 protein and Id1 gene, whereas treatment with Cv2 conversely inhibited Smad1/5/8 activation and Id1 expression, leading to increased generation of cardiac cells. RNA interference-mediated knockdown (KD) of endogenous Cv2 showed increased Smad1/5/8 activation and impaired cardiomyocyte differentiation. Expression of cardiac mesoderm markers was reduced, whereas expression of Id1 and endoderm markers such as Sox7, Hnf4, and E-cadherin was induced in Cv2-kinase dead cells. These phenotypes were rescued by the addition of Cv2 protein to the culture media during the first 2 days of differentiation or co-culture with parental cells. These data suggest that Cv2 may specify cardiac mesodermal lineage through inhibition of BMP signaling at early stage of cardiogenesis.

    DOI: 10.1074/jbc.M801485200

    Web of Science

    researchmap

  • MURC, a muscle-restricted coiled-coil protein, is involved in the regulation of skeletal myogenesis

    Masashi Tagawa, Tomomi Ueyama, Takehiro Ogata, Naofumi Takehara, Norio Nakajima, Koji Isodono, Satoshi Asada, Tomosaburo Takahashi, Hiroaki Matsubara, Hidemasa Oh

    AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY   295 ( 2 )   C490 - C498   2008年8月

     詳細を見る

    記述言語:英語   出版者・発行元:AMER PHYSIOLOGICAL SOC  

    Skeletal myogenesis is a multistep process by which multinucleated mature muscle fibers are formed from undifferentiated, mononucleated myoblasts. However, the molecular mechanisms of skeletal myogenesis have not been fully elucidated. Here, we identified muscle-restricted coiled-coil (MURC) protein as a positive regulator of myogenesis. In skeletal muscle, MURC was localized to the cytoplasm with accumulation in the Z-disc of the sarcomere. In C2C12 myoblasts, MURC expression occurred coincidentally with myogenin expression and preceded sarcomeric myosin expression during differentiation into myotubes. RNA interference (RNAi)-mediated knockdown of MURC impaired differentiation in C2C12 myoblasts, which was accompanied by impaired myogenin expression and ERK activation. Overexpression of MURC in C2C12 myoblasts resulted in the promotion of differentiation with enhanced myogenin expression and ERK activation during differentiation. During injury-induced muscle regeneration, MURC expression increased, and a higher abundance of MURC was observed in immature myofibers compared with mature myofibers. In addition, ERK was activated in regenerating tissue, and ERK activation was detected in MURC-expressing immature myofibers. These findings suggest that MURC is involved in the skeletal myogenesis that results from modulation of myogenin expression and ERK activation. MURC may play pivotal roles in the molecular mechanisms of skeletal myogenic differentiation.

    DOI: 10.1152/ajpcell.00188.2008

    Web of Science

    researchmap

  • MURC, a muscle-restricted coiled-coil protein that modulates the Rho/ROCK pathway, induces cardiac dysfunction and conduction disturbance

    Takehiro Ogata, Tomomi Ueyama, Koji Isodono, Masashi Tagawa, Naofumi Takehara, Tsuneaki Kawashima, Koichiro Harada, Tomosaburo Takahashi, Tetsuo Shioi, Hiroaki Matsubara, Hidemasa Oh

    MOLECULAR AND CELLULAR BIOLOGY   28 ( 10 )   3424 - 3436   2008年5月

     詳細を見る

    記述言語:英語   出版者・発行元:AMER SOC MICROBIOLOGY  

    We identified a novel muscle-restricted putative coiled-coil protein, MURC, which is evolutionarily conserved from frog to human. MURC was localized to the cytoplasm with accumulation in the Z-line of the sarcomere in the murine adult heart. MURC mRNA expression in the heart increased during the developmental process from the embryonic stage to adulthood. In response to pressure overload, MURC mRNA expression increased in the hypertrophied heart. Using the yeast two-hybrid system, we identified the serum deprivation response (SDPR) protein, a phosphatidylserine-binding protein, as a MURC-binding protein. MURC induced activation of the RhoA/ROCK pathway, which modulated serum response factor-mediated atrial natriuretic peptide (ANP) expression and myofibrillar organization. SDPR augmented MURC-induced transactivation of the ANP promoter in cardiomyocytes, and RNA interference of SDPR attenuated the action of MURC on the ANP promoter. Transgenic mice expressing cardiac-specific MURC (Tg-MURC) exhibited cardiac contractile dysfunction and atrioventricular (AV) conduction disturbances with atrial chamber enlargement, reduced thickness of the ventricular wall, and interstitial fibrosis. Spontaneous episodes of atrial fibrillation and AV block were observed in Tg-MURC mice. These findings indicate that MURC modulates RhoA signaling and that MURC plays an important role in the development of cardiac dysfunction and conduction disturbance with increased vulnerability to atrial arrhythmias.

    DOI: 10.1128/MCB.02186-07

    Web of Science

    researchmap

  • Skeletal muscle-derived progenitors capable of differentiating into cardiomyocytes proliferate through myostatin-independent TGF-beta family signaling

    Tetsuya Nomura, Tomomi Ueyama, Eishi Ashihara, Kento Tateishi, Satoshi Asada, Norio Nakajima, Koji Isodono, Tomosaburo Takahashi, Hiroaki Matsubara, Hidemasa Oh

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   365 ( 4 )   863 - 869   2008年1月

     詳細を見る

    記述言語:英語   出版者・発行元:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    The existence of skeletal muscle-derived stem cells (MDSCs) has been suggested in mammals; however, the signaling pathways controlling MDSC proliferation remain largely unknown. Here we report the isolation of myosphere-derived progenitor cells (MDPCs) that can give rise to beating cardiomyocytes from adult skeletal muscle. We identified that follistatin, an antagonist of TGF-beta family members, was predominantly expressed in MDPCs, whereas myostatin was mainly expressed in myogenic cells and mature skeletal muscle. Although follistatin enhanced the replicative growth of MDPCs through Smad2/3 inactivation and cell cycle progression, disruption of myostatin did not increase the MDPC proliferation. By contrast, inhibition of activin A (ActA) or growth differentiation factor 11 (GDF11) signaling dramatically increased MDPC proliferation via down-regulation of p21 and increases in the levels of cdk2/4 and cyclin D1. Thus, follistatin may be an effective progenitor-enhancing agent neutralizing ActA and GDF11 signaling to regulate the growth of MDPCs in skeletal muscle. (C) 2007 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.bbrc.2007.11.087

    Web of Science

    researchmap

  • Downregulation of Dicer expression by serum withdrawal sensitizes human endothelial cells to apoptosis.

    Asada S, Takahashi T, Isodono K, Adachi A, Imoto H, Ogata T, Ueyama T, Matsubara H, Oh H

    Am J Physiol Heart Circ Physiol.   52 ( 23 )   H2512-H2521   2008年

  • 心臓内幹細胞の特性と自己複製制御機構

    王 英正, 立石健人, 松原弘明

    実験医学 増刊号   2008年

     詳細を見る

  • 心不全への再生医療

    足立淳郎, 井本裕子, 山口真一郎, 竹原有史, 王 英正, 松原弘明

    心不全診療マニュアル   2008年

     詳細を見る

  • 心臓組織内幹細胞を用いた心不全への心筋再生医療の現状

    王 英正

    心電図   2008年

     詳細を見る

  • Therapeutic potential of stem/progenitor cells in human skeletal muscle for cardiovascular regeneration

    Tetsuya Nomura, Eishi Ashihara, Kento Tateishi, Tomomi Ueyama, Tomosaburo Takahashi, Masaaki Yamagishi, Toshikazu Kubo, Hitoshi Yaku, Hiroaki Matsubara, Hidemasa Oh

    Current Stem Cell Research and Therapy   2 ( 4 )   293 - 300   2007年12月

     詳細を見る

    記述言語:英語   掲載種別:書評論文,書評,文献紹介等  

    Although myoblast transplantation in patients with ischemic heart failure results in a significant improvement of cardiac function, subsequent studies have consistently shown the myotubes formation in the absence of electromechanical coupling with the neighboring host myocardium, accompanied with the short-term release of paracrine effectors from implanted cells. One major pitfall of using myoblasts is that transplanted cells do not differentiate into cardiomyocytes, which may cause the inherent proarrhythmogenic events. Therefore, whether a discrete subpopulation in heterogeneous muscle-cell cultures is responsible for substantial cardiovascular regeneration has yet to be investigated. We describe here the isolation of progenitor cells from human skeletal muscle. These cells proliferated as non-adherent myospheres in suspension and displayed early embryonic factors and mesenchymal cell-like characteristics. Flow cytometric analyses demonstrated that CD56/N-CAM/Leu-19, a neural cell adhesion molecule abundantly present in myoblasts, was absent in myospheres but was expressed in an adherent cell population containing myogenic precursors. Myosphere-derived progenitor cells (MDPCs) differentiated in culture to produce cardiac, smooth muscle, and endothelial cells. Transplantation of MDPCs into ischemic hearts in NOD/scid mice promoted angiogenesis with substantial cardiovascular regeneration. Our results provide a foundation to further study the cell and biological function of human MDPCs which may have potential therapeutic implications. © 2007 Bentham Science Publishers Ltd.

    DOI: 10.2174/157488807782793808

    Scopus

    PubMed

    researchmap

  • Stage-specific role of endogenous Smad2 activation in cardiomyogenesis of embryonic stem cells

    Ryoji Kitamura, Tomosaburo Takahashi, Norio Nakajima, Koji Isodono, Satoshi Asada, Hikaru Ueno, Tomomi Ueyama, Toshikazu Yoshikawa, Hiroaki Matsubara, Hidemasa Oh

    CIRCULATION RESEARCH   101 ( 1 )   78 - 87   2007年7月

     詳細を見る

    記述言語:英語   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    The role of Smads and their specific ligands during cardiomyogenesis in ES cells was examined. Smad2 was activated bimodally in the early and late phases of cardiac differentiation, whereas Smad1 was activated after the middle phase. Nodal and Cripto were expressed in the early stage and then downregulated, whereas transforming growth factor-beta and activin were expressed only in the late phase. Suppression of early Smad2 activation by SB- 431542 produced complete inhibition of endodermal and mesodermal induction but augmented neuroectodermal differentiation, followed by poor cardiomyogenesis, whereas inhibition during the late phase alone promoted cardiomyogenesis. Inhibitory effect of Smad2 on cardiomyogenesis in the late phase was mainly mediated by transforming growth factor-beta, and inhibition of transforming growth factor-beta- mediated Smad2 activation resulted in a greater replicative potential in differentiated cardiac myocytes and enhanced differentiation of nonmyocytes into cardiac myocytes. Thus, endogenous Smad2 activation is indispensable for endodermal and mesodermal induction in the early phase. In the late phase, endogenous transforming growth factor-beta negatively regulates cardiomyogenesis through Smad2 activation by modulating proliferation and differentiation of cardiac myocytes.

    DOI: 10.1161/CIRCRESAHA.106.147264

    Web of Science

    researchmap

  • Osteopontin is a myosphere-derived secretory molecule that promotes angiogenic progenitor cell proliferation through the phosphoinositide 3-kinase/Akt pathway

    Takehiro Ogata, Tomomi Ueyama, Tetsuya Nomura, Satoshi Asada, Masashi Tagawa, Tomoyuki Nakamura, Tomosaburo Takahashi, Hiroaki Matsubara, Hidemasa Oh

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   359 ( 2 )   341 - 347   2007年7月

     詳細を見る

    記述言語:英語   出版者・発行元:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    We have reported that skeletal myosphere-derived progenitor cells (MDPCs) can differentiate into vascular cells, and that MDPC transplantation into cardiomyopathic hearts improves cardiac function. However, the autocrine/paracrine molecules and underlying mechanisms responsible for MDPC growth have not yet been determined. To explore the molecules enhancing the proliferation of MDPCs, we performed serial analysis of gene expression and signal sequence trap methods using RNA isolated from MDPCs. We identified osteopontin (OPN), a secretory molecule, as one of most abundant molecules expressed in MDPCs. OPN provided a proliferative effect for MDPCs. MDPCs treated with OPN showed Akt activation, and inhibition of the phosphoinositide 3-kinase (PI3K)/Akt pathway repressed the proliferative effect of OPN. Furthermore, OPN-pretreated MDPCs maintained their differentiation potential into endothelial and vascular smooth muscle cells. These findings indicate an important role of OPN as an autocrine/paracrine molecule in regulating the proliferative growth of muscle-derived angiogenic progenitor cells via the PI3K/Akt pathway. (c) 2007 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.bbrc.2007.05.104

    Web of Science

    researchmap

  • Clonally amplified cardiac stem cells are regulated by Sca-1 signaling for efficient cardiovascular regeneration

    Kento Tateishi, Eishi Ashihara, Naofumi Takehara, Tetsuya Nomura, Shoken Honsho, Takuo Nakagami, Shigehiro Morikawa, Tomosaburo Takahashi, Tomomi Ueyama, Hiroaki Matsubara, Hidemasa Oh

    JOURNAL OF CELL SCIENCE   120 ( 10 )   1791 - 1800   2007年5月

     詳細を見る

    記述言語:英語   出版者・発行元:COMPANY OF BIOLOGISTS LTD  

    Recent studies have shown that cardiac stem cells (CSCs) from the adult mammalian heart can give rise to functional cardiomyocytes; however, the definite surface markers to identify a definitive single entity of CSCs and the molecular mechanisms regulating their growth are so far unknown. Here, we demonstrate a single-cell deposition analysis to isolate individually selected CSCs from adult murine hearts and investigate the signals required for their proliferation and survival. Clonally proliferated CSCs express stem cell antigen-1 (Sca-1) with embryonic stem (ES) cell-like and mesenchymal cell-like characteristics and are associated with telomerase reverse transcriptase (TERT). Using a transgene that expresses a GFP reporter under the control of the TERT promoter, we demonstrated that TERTGFP-positive fractions from the heart were enriched for cells expressing Sca-1. Knockdown of Sca-1 transcripts in CSCs led to retarded ex vivo expansion and apoptosis through Akt inactivation. We also show that ongoing CSC proliferation and survival after direct cellgrafting into ischemic myocardium require Sca-1 to upregulate the secreted paracrine effectors that augment neoangiogenesis and limit cardiac apoptosis. Thus, Sca-1 might be an essential component to promote CSC proliferation and survival to directly facilitate early engraftment, and might indirectly exert the effects on late cardiovascular differentiation after CSC transplantation.

    DOI: 10.1242/jcs.006122

    Web of Science

    researchmap

  • Skeletal myosphere-derived progenitor cell transplantation promotes neovascularization in delta-sarcoglycan knockdown cardiomyopathy

    Tetsuya Nomura, Eishi Ashihara, Kento Tateishi, Satoshi Asada, Tomomi Ueyama, Tomosaburo Takahashi, Hiroaki Matsubara, Hidemasa Oh

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   352 ( 3 )   668 - 674   2007年1月

     詳細を見る

    記述言語:英語   出版者・発行元:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    Bone marrow cells have been shown to contribute to neovascularization in ischemic hearts, whereas their impaired maturation to restore the delta-sarcoglycan (delta-SG) expression responsible for focal myocardial degeneration limits their utility to treat the pathogenesis of cardiomyopathy. Here, we report the isolation of multipotent progenitor cells from adult skeletal muscle, based on their ability to generate floating-myospheres. Myosphere-derived progenitor cells (MDPCs) are distinguishable from myogenic C2C12 cells and differentiate into vascular smooth muscle cells and mesenchymal progeny. The mutation in the delta-SG has been shown to develop vascular spasm to affect sarcolemma structure causing cardiomyopathy. We originally generated delta-SD knockdown (KD) mice and transplanted MDPCs into the hearts. MDPCs enhanced neoangiogenesis and restored delta-SG expression in impaired vasculatures through trans-differentiation, leading to improvement of cardiac function associated with paracrine effectors secretion. We propose that MDPCs may be the promising progenitor cells in skeletal muscle to treat delta-sarcoglycan complex mutant cardiomyopathy. (c) 2006 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.bbrc.2006.11.097

    Web of Science

    researchmap

  • Human cardiac stem cells exhibit mesenchymal features and are maintained through Akt/GSK-3 beta signaling

    Kento Tateishi, Eishi Ashihara, Shoken Honsho, Naofumi Takehara, Tetsuya Nomura, Tomosaburo Takahashi, Tomomi Ueyama, Masaaki Yamagishi, Hitoshi Yaku, Hiroaki Matsubara, Hidemasa Oh

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   352 ( 3 )   635 - 641   2007年1月

     詳細を見る

    記述言語:英語   出版者・発行元:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    Recent evidence suggested that human cardiac stem cells (hCSCs) may have the clinical application for cardiac repair; however, their characteristics and the regulatory mechanisms of their growth have not been fully investigated. Here, we show the novel property of hCSCs with respect to their origin and tissue distribution in human heart, and demonstrate the signaling pathway that regulates their growth and survival. Telomerase-active hCSCs were predominantly present in the right atrium and outflow tract of the heart (infant > adult) and had a mesenchymal cell-like phenotype. These hCSCs expressed the embryonic stem cell markers and differentiated into cardio-myocytes to support cardiac function when transplanted them into ischemic myocardium. Inhibition of Akt pathway impaired the hCSC proliferation and induced apoptosis, whereas inhibition of glycogen synthase kinase-3 (GSK-3) enhanced their growth and survival. We conclude that hCSCs exhibit mesenchymal features and that Akt/GSK-3 beta may be crucial modulators for hCSC maintenance in human heart. (c) 2006 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.bbrc.2006.11.096

    Web of Science

    researchmap

  • ヒト心筋組織幹細胞研究の現状

    王 英正

    分子血管病   2007年

     詳細を見る

  • 心筋細胞の再生医療

    王 英正

    メディカルビューポイント   2007年

     詳細を見る

  • Isl-1前駆細胞

    王 英正

    Annual Review 循環器   2007年

     詳細を見る

  • 心臓幹細胞移植による臨床応用の可能性

    王 英正

    呼吸と循環   2007年

     詳細を見る

▼全件表示

講演・口頭発表等

  • Cell therapy trials in congenital heart disease

    日本遺伝子細胞治療学会  2018年 

     詳細を見る

  • Cell Therapy Trials in Congenital Heart Disease

    Pediatric Heart Disease Symposium  2017年 

     詳細を見る

  • 心筋組織幹細胞を用いた心筋再生の現状と展望

    CVIT  2017年 

     詳細を見る

  • Cell therapy trials in congenital heart disease

    日本遺伝子細胞治療学会  2017年 

     詳細を見る

  • 先駆け審査制度での成功事例 自家心臓内幹細胞/小児心不全に対する心筋再生医療法の企業主導多施設共同臨床治験

    AMED シンポジウム 革新的医療技術創出プロジェクト  2017年 

     詳細を見る

  • カテーテルによる心筋再生医療について

    日本IVR学会総会  2017年 

     詳細を見る

  • Cardiac Progenitor Cell Therapy in Congenital Heart Diseases

    第80回日本循環器学会学術集会  2016年 

     詳細を見る

  • Cardiac progenitor cell therapy in congenital heart disease

    American Heart Association  2016年 

     詳細を見る

  • 先天性心疾患における心筋再生医療の実用化研究

    第119回小児科学会シンポジウム  2016年 

     詳細を見る

  • Cardiac progenitor cell therapy for congenital heart diseases

    3rd Munich Conference on Cardiac Development  2016年 

     詳細を見る

  • 心筋再生医療の現状と展望

    Cardiovascular Update 岡山  2015年 

     詳細を見る

  • 疾患特異的iPS細胞による新たな先天性心疾患モデルの作成

    小児循環器学会  2015年 

     詳細を見る

  • 小児心不全に対する心筋再生医療法の企業主導多施設共同臨床治験

    橋渡し研究シンポジウム  2015年 

     詳細を見る

  • 心不全に対する細胞治療法の実用化と医工学融合した次世代心筋再生医療法の開発

    岡山先端医学研究会  2015年 

     詳細を見る

  • 小児心不全に対する心臓内自己幹細胞移植治療の標準医療化に向けた取り組み

    小児循環器学会  2015年 

     詳細を見る

  • 心臓内幹細胞を用いた先天性心疾患の病態解明と再生医療

    ミニリトリート 徳島  2015年 

     詳細を見る

  • 子どもの心臓病に再生医療は有効か?

    岡山大学公開講座  2015年 

     詳細を見る

  • 心臓内幹細胞を用いた小児心疾患の解明と再生医療

    第34回日本小児病理研究会学術集会  2014年 

     詳細を見る

  • 左心低形成症候群に対する心筋再生医療の第1/2相臨床研究

    日本小児循環器学会  2014年 

     詳細を見る

  • iPS細胞を用いた左心低形成症候群における疾患発症機序の解明

    日本小児循環器学会  2014年 

     詳細を見る

  • 先天性心疾患への再生医療の現状

    抗加齢医学会総会  2014年 

     詳細を見る

  • 心臓内幹細胞を用いた小児心疾患の解明と再生医療

    高知小児循環器・川崎病研究会  2014年 

     詳細を見る

  • 臨床試験における具体的な評価指標の定め方

    技術情報協会セミナー  2014年 

     詳細を見る

  • 小児心不全に対する心臓内幹細胞自家移植療法の第I/II相臨床研究

    第56回日本小児血液・がん学会学術集会  2014年 

     詳細を見る

  • 希少難治性心不全に対する心臓内幹細胞を用いた再生医療

    岡山大学知恵の見本市2013  2013年 

     詳細を見る

  • 心不全への幹細胞移植療法

    岡山先端医学研究会  2013年 

     詳細を見る

  • 心不全への幹細胞移植療法

    第3回先端医学研究会at OU  2013年 

     詳細を見る

  • 先天性心疾患に対する自己心臓内幹細胞による再生医療

    第116回日本小児科学会学術集会  2013年 

     詳細を見る

  • Intracoronary delivery of cardiac progenitor cells in patients with hypoplastic left heart syndrome.

    The 30th International Society for Heart Research  2013年 

     詳細を見る

  • 希少難治性心不全に対する心臓内幹細胞を用いた再生医療

    青森臨床循環器研究会  2013年 

     詳細を見る

  • 希少難治性心不全に対するヒト幹細胞移植療法の長期的エビデンス

    第12回日本再生医療学会  2013年 

     詳細を見る

  • 疾患特異的幹細胞およびiPS細胞を駆使した希少小児心疾患に対する細胞治療と病態解明

    消化器研究セミナー  2013年 

     詳細を見る

  • iPS細胞を用いた心疾患の新たな診断法と治療開発

    岡山大学サイエンスカフェ  2013年 

     詳細を見る

  • 子どもの難治性心不全に対する幹細胞移植療法の取り組み

    公開セミナーはあとネット兵庫  2013年 

     詳細を見る

  • Mechanical stretch promotes reprogramming of human cardiac progenitors into functional cardiomyocytes by defined factors.

    日本循環器学会  2012年 

     詳細を見る

  • 心筋再生医療の臨床試験と研究開発状況

    技術情報協会セミナー  2012年 

     詳細を見る

  • Cardiac progenitor cell infusion in patients with hypoplastic left heart syndrome: a prospective phase 1 clinical trial

    Japanese Heart Failure Society  2012年 

     詳細を見る

  • 重度心臓病に対する心筋再生医療

    オープンフォーラム2012 岡山  2012年 

     詳細を見る

  • Mending and Modeling the Congenital Heart Diseases by Patient-Specific Cardiac Progenitors.

    Symposium at Texas Heart Institute  2012年 

     詳細を見る

  • 小児心不全への再生医療の可能性

    第15回遺伝子治療推進産学懇話会  2012年 

     詳細を見る

  • Mending and Modeling the Congenital Heart Diseases by Patient-Specific Cardiac Progenitors

    東京女子医科大学セミナー  2012年 

     詳細を見る

  • 左心低形成症候群に対する心臓内幹細胞自家移植療法

    第7回岡山心移植心不全研究会  2012年 

     詳細を見る

  • 小児心不全と細胞治療

    先天性心疾患シンポジウム  2012年 

     詳細を見る

  • 小児心不全に対する細胞治療の中間報告と疾患特異的iPS細胞の樹立による次世代心臓再生法の開発

    橋渡し研究加速推進ネットワークシンポジウム  2012年 

     詳細を見る

  • 先天性心疾患患者由来の心臓内幹細胞を用いた疾患特異的ヒトiPS細胞の樹立と機能解析.

    日本小循環器学会  2012年 

     詳細を見る

  • Heterokaryon-based reprogramming of human cardiac progenitor cells into functional cardiomyocytes.

    日本小循環器学会  2012年 

     詳細を見る

  • Mechanical stretch modulates calcium handling during direct cardiac reprogramming of resident progenitor cells in human heart.

    国際幹細胞学会  2012年 

     詳細を見る

  • Transition of cardiogenic to angiogeneic potential of human cardiac progenitor cells occurs with age.

    国際幹細胞学会  2012年 

     詳細を見る

  • Patient-specific induced pluripotent stem cells from cardiac progenitors recapitulate the models for cardiac chamber disorders.

    欧州心臓病学会  2012年 

     詳細を見る

  • Mechanical stretch modulates calcium handling during direct cardiac reprogramming of resident progenitor cells in human heart.

    欧州心臓病学会  2012年 

     詳細を見る

  • 小児心不全に対する細胞治療の中間報告と疾患特異的iPS細胞の樹立による次世代心臓再生法の開発

    橋渡し研究加速推進ネットワークシンポジウム  2012年 

     詳細を見る

  • 小児心不全への細胞治療法の可能性

    岡山心臓血管外科カンファレンス  2012年 

     詳細を見る

  • Mending and Modeling the Congenital Heart Diseases by Patient-Specific Cardiac Progenitors

    2012年 

     詳細を見る

  • Patient-specific induced pluripotent stem cells from cardiac progenitors recapitulate the models for cardiac chamber disorder.

    国際幹細胞学会  2012年 

     詳細を見る

  • Reprogramming of human cardiac progenitors into pluripotency in patients with congenital heart disease.

    日本循環器学会  2012年 

     詳細を見る

  • 小児心不全と細胞治療

    先天性心疾患シンポジウム  2012年 

     詳細を見る

  • 心不全の心筋再生医療

    岡二会  2012年 

     詳細を見る

  • Generation and functional analysis of induced pluripotent stem cells in patients with congenital heart disease.

    日本胸部外科学会  2011年 

     詳細を見る

  • Insulin-like growth factor-2 receptor controls human cardiac progenitor proliferation and differentiation in children with congenital heart malformation.

    米国心臓病学会  2011年 

     詳細を見る

  • 小児心不全への細胞治療の現状と展望

    重症心不全治療フォーラム  2011年 

     詳細を見る

  • Direct induction of human cardiac progenitor cells to functional cardiomyocytes by defined factors.

    米国心臓病学会  2011年 

     詳細を見る

  • Heterokaryon-based reprogramming of human cardiac progenitor cells into functional cardiomyocytes.

    日本胸部外科学会  2011年 

     詳細を見る

  • Direct reprogramming of human cardiac progenitor cells towards functional cardiomyocytes.

    日本胸部外科学会  2011年 

     詳細を見る

▼全件表示

Works(作品等)

  • 2012見本市

    2012年

     詳細を見る

    作品分類:芸術活動  

    researchmap

受賞

  • 文部科学大臣表彰科学技術賞

    2012年  

     詳細を見る

    受賞国:日本国

    researchmap

 

担当授業科目

  • 心筋梗塞特論 (2021年度) 特別  - その他