研究者詳細 - 山本　健一

論文 - 山本　健一

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Periostin in Allergic Inflammation 査読

Kenji Izuhara, Kazuhiko Arima, Shoichiro Ohta, Shoichi Suzuki, Masako Inamitsu, Ken-ichi Yamamoto

ALLERGOLOGY INTERNATIONAL 63 ( 2 ) 143 - 151 2014年6月

記述言語：英語出版者・発行元：JAPANESE SOCIETY ALLERGOLOGY

Periostin, an extracellular matrix protein belonging to the fasciclin family, has been shown to play a critical role in the process of remodeling during tissue/organ development or repair. Periostin functions as a matricellular protein in cell activation by binding to their receptors on cell surface, thereby exerting its biological activities. After we found that periostin is a downstream molecule of interleukin (IL)-4 and IL-13, signature cytokines of type 2 immune responses, we showed that periostin is a component of subepithelial fibrosis in bronchial asthma, the first formal proof that periostin is involved in allergic inflammation. Subsequently, a great deal of evidence has accumulated demonstrating the significance of periostin in allergic inflammation. It is of note that in skin tissues, periostin is critical for amplification and persistence of allergic inflammation by communicating between fibroblasts and keratinocytes. Furthermore, periostin has been applied to development of novel diagnostics or therapeutic agents for allergic diseases. Serum periostin can reflect local production of periostin in inflamed lesions induced by Th2-type immune responses and also can predict the efficacy of Th2 antagonists against bronchial asthma. Blocking the interaction between periostin and its receptor, alpha(v) integrin, or down-regulating the periostin expression shows improvement of periostin-induced inflammation in mouse models or in in vitro systems. It is hoped that diagnostics or therapeutic agents targeting periostin will be of practical use in the near future.

DOI： 10.2332/allergolint.13-RAI-0663

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Periostin controls keratinocyte proliferation and differentiation by interacting with the paracrine IL-1α/IL-6 loop 査読

Journal of Investigative Dermatology 134 ( 5 ) 1295 - 1304 2014年5月

Asthma 査読

Kenji Izuhara, Shoichi Suzuki, Kazuhiko Arima, Shoichiro Ohta, Masako Inamitsu, Ken-Ichi Yamamoto

Metabolism of Human Diseases: Organ Physiology and Pathophysiology 215 - 219 2014年1月

記述言語：英語掲載種別：論文集(書籍)内論文出版者・発行元：Springer-Verlag Wien

Asthma is one of the most common chronic diseases, with an estimated 300 million people affected worldwide [ 1 ]. The incidence of asthma continues to increase, especially among children. Asthmais defi ned by its clinical, physiological, and pathological characteristics [ 1 ]. Its predominant clinical feature is recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. The main physiological feature is episodic obstructed breathing characterized by constricted expiratory airways, leading to asthma’s clinical features.The dominant pathological feature is chronic infl ammation of the airways associated with airway hyperresponsiveness, which obstructs or limits airfl ow when airways are exposed to various risk factors.Chronic inflammation is characterized as infi ltration of infl ammatory cells (e.g., mast cells, eosinophils, and T cells
see chapter “ Overview ” under the part “Immune system”) and is sometimes associated with airway structural changes called “remodeling”such as mucus hyperproduction by epithelial cells, subepithelial fi brosis by fi broblasts, hypertrophy and/or hyperplasia of airway smooth muscle cells, and proliferation of blood vessels.

DOI： 10.1007/978-3-7091-0715-7_32

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[Application of basic research to development of diagnostics and therapeutic agents against inflammatory diseases]. 査読

Kenji Izuhara, Shoichiro Ohta, Kazuhiko Arima, Shoichi Suzuki, Masako Inamitsu, Ken-ichi Yamamoto

Rinsho byori. The Japanese journal of clinical pathology 61 ( 10 ) 900 - 8 2013年10月

記述言語：日本語

Biomarkers are generally important for the treatment of patients from the points of diagnosis of disease, assessment of cure, assessment of prognosis such as metastasis or recurrence, prevention of disease, and prediction of drug efficacy. Currently it is well accepted that allergic diseases such as bronchial asthma and atopic dermatitis are not single diseases, but syndromes encompassing different diseases entities. Therefore, it is important to cluster allergic disease patients to assess prognosis or the choice of therapeutic drugs, and useful biomarkers are required for these purposes. Periostin, an extracellular matrix protein, has recently emerged as a biomarker useful for clustering asthma patients. We further found that periostin plays an important role in allergic inflammation and based on this finding we are now developing therapeutic agents targeting periostin against allergic diseases. Since periostin is involved in the pathogenesis of various inflammatory diseases in addition to allergic diseases, such diagnostics and therapeutic agents can be applied to many inflammatory diseases. In this article, we describe the history of periostin research and our application of basic research to the development of diagnostics and therapeutic agents against inflammatory diseases.

PubMed

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Inhibition of RAGE signaling through the intracellular delivery of inhibitor peptides by PEI cationization 査読

Endy Widya Putranto, Hitoshi Murata, Ken-Ichi Yamamoto, Ken Kataoka, Hidenori Yamada, Jun-Ichiro Futami, Masakiyo Sakaguchi, Nam-Ho Huh

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 32 ( 4 ) 938 - 944 2013年10月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：SPANDIDOS PUBL LTD

The receptor for advanced glycation end products (RAGE) is a multi-ligand cell surface receptor and a member of the immunoglobulin superfamily. RAGE is involved in a wide range of inflammatory, degenerative and hyper-proliferative disorders which span over different organs by engaging diverse ligands, including advanced glycation end products, S100 family proteins, high-mobility group protein B1 (HMGB1) and amyloid beta. We previously demonstrated that the cytoplasmic domain of RAGE is phosphorylated upon the binding of ligands, enabling the recruitment of two distinct pairs of adaptor proteins, Toll-interleukin 1 receptor domain-containing adaptor protein (TIRAP) and myeloid differentiation protein 88 (MyD88). This engagement allows the activation of downstream effector molecules, and thereby mediates a wide variety of cellular processes, such as inflammatory responses, apoptotic cell death, migration and cell growth. Therefore, inhibition of the binding of TIRAP to RAGE may abrogate intracellular signaling from ligand-activated RAGE. In the present study, we developed inhibitor peptides for RAGE signaling (RAGE-I) by mimicking the phosphorylatable cytosolic domain of RAGE. RAGE-I was efficiently delivered into the cells by polyethylenimine (PEI) cationization. We demonstrated that RAGE-I specifically bound to TIRAP and abrogated the activation of Cdc42 induced by ligand-activated RAGE. Furthermore, we were able to reduce neuronal cell death induced by an excess amount of S100B and to inhibit the migration and invasion of glioma cells in vitro. Our results indicate that RAGE-I provides a powerful tool for therapeutics to block RAGE-mediated multiple signaling.

DOI： 10.3892/ijmm.2013.1467

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DOCK7 is a critical regulator of the RAGE-Cdc42 signaling axis that induces formation of dendritic pseudopodia in human cancer cells 査読

Ken-Ichi Yamamoto, Hitoshi Murata, Endy Widya Putranto, Ken Kataoka, Akira Motoyama, Toshihiko Hibino, Yusuke Inoue, Masakiyo Sakaguchi, Nam-Ho Huh

ONCOLOGY REPORTS 29 ( 3 ) 1073 - 1079 2013年3月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：SPANDIDOS PUBL LTD

Cellular migration is a fundamental process linked to cancer metastasis. Growing evidence indicates that the receptor for advanced glycation end products (RAGE) plays a pivotal role in this process. With regard to downstream signal transducers of RAGE, diaphanous-1 and activated small guanine nucleotide triphosphatases, Rac1 and Cdc42, have been identified. To obtain precise insight into the direct downstream signaling mechanism of RAGE, we screened for proteins interacting with the cytoplasmic domain of RAGE employing an immunoprecipitation-liquid chromatography coupled with an electrospray tandem mass spectrometry system. In the present study, we found that the cytoplasmic domain of RAGE interacted with an atypical DOCK180-related guanine nucleotide exchange factor, dedicator of cytokinesis protein 7 (DOCK7). DOCK7 bound to the RAGE cytoplasmic domain and transduced a signal to Cdc42, resulting in the formation of abundant highly branched filopodia-like protrusions, dendritic pseudopodia. Blocking of the function of DOCK7 greatly abrogated the formation of dendritic pseudopodia and suppressed cellular migration. These results indicate that DOCK7 functions as an essential and downstream regulator of RAGE-mediated cellular migration through the formation of dendritic pseudopodia.

DOI： 10.3892/or.2012.2191

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S100A7 promotes the migration and invasion of osteosarcoma cells via the receptor for advanced glycation end products 査読

Ken Kataoka, Tomoyuki Ono, Hitoshi Murata, Mika Morishita, Ken-Ichi Yamamoto, Masakiyo Sakaguchi, Nam-Ho Huh

ONCOLOGY LETTERS 3 ( 5 ) 1149 - 1153 2012年5月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：SPANDIDOS PUBL LTD

Osteosarcoma is the most common malignant tumor of bone in childhood and adolescence. Despite intensive research for new therapies, the outcome in patients with metastasis remains extremely poor. S100 proteins are involved in the proliferation, cell cycle progression and metastasis of numerous malignant tumors, including osteosarcoma. In the present study, we identified S100A7 as a candidate to promote the migration of osteosarcoma cells. S100A7 promoted the migration and invasion of osteosarcoma cells as assayed in vitro. An in vitro pull-down assay revealed the binding of the recombinant S100A7 protein with its putative receptor, the receptor for advanced glycation end products (RAGE). The downregulation of RAGE by a specific siRNA markedly suppressed the migration and invasion of osteosarcoma cells. Furthermore, the matrix metalloproteinase activity of osteosarcoma cells was enhanced by S100A7 and suppressed by the downregulation of RAGE. These results indicate that S100A7 promotes the migration and invasion of osteosarcoma cells through RAGE. The S100A7-RAGE axis may thus be a new target for preventing the invasion and/or metastasis of osteosarcoma.

DOI： 10.3892/ol.2012.612

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TIRAP, an Adaptor Protein for TLR2/4, Transduces a Signal from RAGE Phosphorylated upon Ligand Binding 査読

Masakiyo Sakaguchi, Hitoshi Murata, Ken-ichi Yamamoto, Tomoyuki Ono, Yoshihiko Sakaguchi, Akira Motoyama, Toshihiko Hibino, Ken Kataoka, Nam-ho Huh

PLOS ONE 6 ( 8 ) e23132-e23132 2011年8月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：PUBLIC LIBRARY SCIENCE

The receptor for advanced glycation end products (RAGE) is thought to be involved in the pathogenesis of a broad range of inflammatory, degenerative and hyperproliferative diseases. It binds to diverse ligands and activates multiple intracellular signaling pathways. Despite these pivotal functions, molecular events just downstream of ligand-activated RAGE have been surprisingly unknown. Here we show that the cytoplasmic domain of RAGE is phosphorylated at Ser391 by PKCf upon binding of ligands. TIRAP and MyD88, which are known to be adaptor proteins for Toll-like receptor-2 and -4 (TLR2/4), bound to the phosphorylated RAGE and transduced a signal to downstream molecules. Blocking of the function of TIRAP and MyD88 largely abrogated intracellular signaling from ligand-activated RAGE. Our findings indicate that functional interaction between RAGE and TLRs coordinately regulates inflammation, immune response and other cellular functions.

DOI： 10.1371/journal.pone.0023132

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Internalization of REIC/Dkk-3 protein by induced pluripotent stem cell-derived embryoid bodies and extra-embryonic tissues 査読

Ken Kataoka, Masakiyo Sakaguchi, Kun Peng Li, Chika Taketa, Ken-Ichi Yamamoto, Gang Du, Hiroaki Funahashi, Hitoshi Murata, Nam-Ho Huh

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 26 ( 6 ) 853 - 859 2010年12月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：SPANDIDOS PUBL LTD

REIC/Dkk-3 was first identified as a down-regulated gene in a number of human immortalized cells and human tumor-derived cell lines. Overexpression of the REIC/Dkk-3 gene using an adenovirus vector (Ad-REIC) has showed a potent selective therapeutic effect on various human cancers through induction of ER stress. Furthermore, we recently showed that Ad-REIC has an indirect host-mediated anti-tumor activity by induction of IL-7. However, the physiological function of REIC/Dkk-3 is still unclear. As a first step to study the possible receptor(s) for secreted REIC/Dkk-3, we analyzed the internalization of Cy3-labeled recombinant REIC/Dkk-3 protein. Among the cell lines screened, mouse induced pluripotent stem (iPS) cells showed a unique pattern of internalization. The internalization was observed in peripheral cells of spherical colonies formed spontaneously, but not in undifferentiated iPS cells. When we analyzed embryoid bodies (EBs) derived from iPS cells, REIC/Dkk-3 protein was internalized specifically by differentiated cells located at the periphery of EBs. Interestingly, Dkk-1 was internalized by undifferentiated cells at the center of the EBs. When developmental tissue was analyzed, internalization of REIC/Dkk-3 protein was strictly limited to extra-embryonic tissue, such as the trophectoderm layer of 4.5 days post-coitus (dpc) blastocysts and the chorionic membrane at 16.5 dpc. The mechanism of the internalization was confirmed to be endocytosis. These findings will contribute to knowledge on the interaction of REIC/Dkk-3 with a possible receptor(s).

DOI： 10.3892/ijmm_00000534

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Transcriptional regulation of a brown adipocyte-specific gene, UCP1, by KLF11 and KLF15 査読

Ken-ichi Yamamoto, Masakiyo Sakaguchi, Reinhold J. Medina, Aya Niida, Yoshihiko Sakaguchi, Masahiro Miyazaki, Ken Kataoka, Nam-ho Huh

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 400 ( 1 ) 175 - 180 2010年9月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：ACADEMIC PRESS INC ELSEVIER SCIENCE

Several growth factors and transcription factors have been reported to play important roles in brown adipocyte differentiation and modulation of thermogenic gene expression, especially the expression of UCP1. In this study, we focused on KLF11 and KLF15, which were expressed highly in brown adipose tissue. Our data demonstrated that KLF11 and KLF15 interacted directly with the UCP1 promoter using GC-box and GT-boxes, respectively. Co-transfection of KLF11 and KLF15 in the mesenchymal stem cell line muBM3.1 during brown adipocyte differentiation enhanced the expression level of UCP1. KLF11, but not KLF15, was essential for UCP1 expression during brown adipocyte differentiation of muBM3.1. (C) 2010 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.bbrc.2010.08.039

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A Novel Three-Dimensional Culture System for Isolation and Clonal Propagation of Neural Stem Cells Using a Thermo-Reversible Gelation Polymer 査読

Xin-Zhi Yang, Ken Kataoka, Reinhold Medina, Ken-Ichi Yamamoto, Swe Swe Than, Masahiro Miyazaki, Nam-Ho Huh

TISSUE ENGINEERING PART C-METHODS 15 ( 4 ) 615 - 623 2009年12月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：MARY ANN LIEBERT INC

In the present study, we examined the possible utility of a three-dimensional culture system using a thermo-reversible gelation polymer to isolate and expand neural stem cells (NSCs). The polymer is a synthetic biologically inert polymer and gelates at temperatures higher than the gel-sol transition point (similar to 20 degrees C). When fetal mouse brain cells were inoculated into the gel, spherical colonies were formed (similar to 1% in primary culture and similar to 9% in passage cultures). The spheroid-forming cells were positive for expression of the NSC markers nestin and Musashi. Under conditions facilitating spontaneous neural differentiation, the spheroid-forming cells expressed genes characteristic to astrocytes, oligodendrocytes, and neurons. The cells could be successively propagated at least to 80 poly-D-lysines over a period of 20 weeks in the gel culture with a growth rate higher than that observed in suspension culture. The spheroids formed by fetal mouse brain cells in the gel were shown to be of clonal origin. These results indicate that the spheroid culture system is a convenient and powerful tool for isolation and clonal expansion of NSCs in vitro.

DOI： 10.1089/ten.tec.2008.0516

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