研究者詳細 - 王　英正

MISC - 王　英正

分割表示 146 件中 81 - 100 件目／全件表示 >>

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1相試験(TICAP)

樽井俊, 石神修大, 大月審一, 逢坂大樹, 栄徳隆裕, 近藤麻衣子, 小林純子, 奥山倫弘, 馬場健児, 川畑拓也, 吉積功, 黒子洋介, 新井禎彦, 岩崎達雄, 佐藤修平, 笠原真悟, 佐野俊二, 王英正

再生医療 13 2014年

心臓MRIの遅延造影を用いた幼児期単心室症患者における心筋線維化の検出と臨床的意義

逢坂大樹, 石神修大, 奥山倫弘, 小林純子, 樽井俊, 笠原真悟, 佐野俊二, 王英正

日本小児循環器学会雑誌 30 ( Supplement ) 2014年

YT-11-5(YRA) 疾患特異的iPS細胞を用いた左心低形成症候群における心臓発生異常の解明(YT Young Researcher Award & Traveler's Grant,第113回日本外科学会定期学術集会)

小林純子, 樽井俊, 平田昌敬, 川畑拓也, 黒子洋介, 立石篤史, 吉積功, 新井禎彦, 笠原真悟, 佐野俊二, 王英正

日本外科学会雑誌 114 ( 2 ) 415 - 415 2013年3月

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

ハーフクリップ法によるラット右心負荷モデルの作製

奥山倫弘, 平田昌敬, 逢坂大樹, 樽井俊, 小林純子, 笠原真悟, 佐野俊二, 王英正

日本心臓血管外科学会雑誌 42 ( Supplement ) 2013年

Patient-specific Induced Pluripotent Stem Cells For Modeling Hypoplastic Left Heart Syndrome

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

CIRCULATION 126 ( 21 ) 2012年11月

Factors-based Human Cardiomyocytes Differentiation Exhibits Defective Maturation and Excitation Through Aberrant Calcium Handling Proteins

Suguru Tarui, Junko Kobayashi, Masataka Hirata, Ken Takahashi, Gentaro Iribe, Keiji Naruse, Shingo Kasahara, Shunji Sano, Hidemasa Oh

CIRCULATION 126 ( 21 ) 2012年11月

Hedgehog Interacting Protein Controls Age-Dependent Angiogenic Activity in Human Cardiac Progenitor Cells Through Insulin-Like Growth Factor-1 Receptor Signaling

Masashi Yoshida, Suguru Tarui, Junko Kobayashi, Masataka Hirata, Yasufumi Kijima, Tohru Miyoshi, Kazufumi Nakamura, Kengo Kusano, Youhei Maeshima, Shunji Sano, Hiroshi Ito, Hidemasa Oh

CIRCULATION 126 ( 21 ) 2012年11月

Cardiac Progenitor Cell Infusion in Patients with Hypoplastic Left Heart Syndrome: a Prospective Phase 1 Clinical Trial

Hidemasa Oh, Suguru Tarui, Shinichi Otsuki, Shunji Sano

JOURNAL OF CARDIAC FAILURE 18 ( 10 ) S145 - S145 2012年10月

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

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

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

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 ( 1 ) 27 - 34 2012年

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

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

新生児Ebstein奇形のManagement

藤井泰宏, 新井禎彦, 石神修太, 樽井俊, 櫻井茂, 鵜垣伸也, 川畑拓也, 立石篤史, 藤田康文, 高垣昌巳, 平田昌敬, 笠原真悟, 三井秀也, 王英正, 佐野俊二

日本心臓血管外科学会雑誌 40 ( Supplement ) 199 - 199 2011年1月

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

小児心不全に対する心筋再生療法.

樽井俊, 佐野俊二, 王英正

Medical Science Digest 37 ( 11 ) 439 - 442 2011年

MURC, Muscle-Restricted Coiled-Coil Protein, Regulates Caveolae Morphology and Induces Hypertrophy in Cardiomyocytes

Takuya Taniguchi, Takehiro Ogata, Daisuke Naito, Naohiko Nakanishi, Kotaro Miyagawa, Katsuya Amano, Koji Isodono, Hiroko Imoto, Masashi Tagawa, Naofumi Takehara, Satoshi Asada, Atsuo Adachi, Tatsuya Morimoto, Tomosaburo Takahashi, Hidemasa Oh, Tomomi Ueyama, Hiroaki Matsubara

CIRCULATION 122 ( 21 ) 2010年11月

PARM-1 Is an Endoplasmic Reticulum Molecule Involved in Endoplasmic Reticulum Stress-Induced Apoptosis in Rat Cardiac Myocytes

Koji Isodono, Tomosaburo Takahashi, Hiroko Imoto, Naohiko Nakanishi, Takehiro Ogata, Satoshi Asada, Atsuo Adachi, Tomomi Ueyama, Hidemasa Oh, Hiroaki Matsubara

PLOS ONE 5 ( 3 ) e9746-e9746 2010年3月

記述言語：英語出版者・発行元：PUBLIC LIBRARY SCIENCE

To identify novel transmembrane and secretory molecules expressed in cardiac myocytes, signal sequence trap screening was performed in rat neonatal cardiac myocytes. One of the molecules identified was a transmembrane protein, prostatic androgen repressed message-1 (PARM-1). While PARM-1 has been identified as a gene induced in prostate in response to castration, its function is largely unknown. Our expression analysis revealed that PARM-1 was specifically expressed in hearts and skeletal muscles, and in the heart, cardiac myocytes, but not non-myocytes expressed PARM-1. Immunofluorescent staining showed that PARM-1 was predominantly localized in endoplasmic reticulum (ER). In Dahl salt-sensitive rats, high-salt diet resulted in hypertension, cardiac hypertrophy and subsequent heart failure, and significantly stimulated PARM-1 expression in the hearts, with a concomitant increase in ER stress markers such as GRP78 and CHOP. In cultured cardiac myocytes, PARM-1 expression was stimulated by proinflammatory cytokines, but not by hypertrophic stimuli. A marked increase in PARM-1 expression was observed in response to ER stress inducers such as thapsigargin and tunicamycin, which also induced apoptotic cell death. Silencing PARM-1 expression by siRNAs enhanced apoptotic response in cardiac myocytes to ER stresses. PARM-1 silencing also repressed expression of PERK and ATF6, and augmented expression of CHOP without affecting IRE-1 expression and JNK and Caspase-12 activation. Thus, PARM-1 expression is induced by ER stress, which plays a protective role in cardiac myocytes through regulating PERK, ATF6 and CHOP expression. These results suggested that PARM-1 is a novel ER transmembrane molecule involved in cardiac remodeling in hypertensive heart disease.

DOI： 10.1371/journal.pone.0009746

Web of Science

researchmap

Stem Cell Engineering for Cardiac Tissue Regeneration

Masashi Yoshida, Hidemasa Oh

CARDIOLOGY 115 ( 3 ) 191 - 193 2010年

　前のページ - 次のページ　

<王 英正>

MISC - 王 英正

<王　英正>

MISC - 王　英正