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KAWAGISHI Hiroyuki

Academic OrganizationTEL
Education and Research OrganizationSchool of Medicine Department of Molecular PharmacologyFAX
PositionAssociate ProfessorMail Addresskawa13@shinshu-u.ac.jp
Address3-1-1, Asahi, Matsumoto City 390-8621Web sitehttps://www.shinshu-u.ac.jp/institution/ibs/department/bbe.html
http://www.shinshu-u.ac.jp/faculty/medicine/chair/i-yakuri/

Profile

Research Field
Keywords:Senescence , Cancer , Heart
Academic Societies
Academic Societies
日本毒性学会
日本薬学会
日本生理学会
日本基礎老化学会
THE JAPANESE PHARMACOLOGICAL SOCIETY
日本心脈管作動物質学会
Japanese Association of Cardiovascular Pharmacology
THE MOLECULAR BIOLOGY SOCIETY OF JAPAN
International Society for Heart Research
SPS
日本安全性薬理学会
Awards
2022 , Young Investigator Award
2022 , 優秀発表賞
2021 , 研究奨励賞 最優秀賞
2020 , Young Investigator Award
2008 , Young Investigator Award
Research Career
Overseas Education
2012-2017 , National Heart, Lung and Blood Institute/NIH

Research

Books, Articles, etc.
Books
細胞老化と組織老化, 老年医学(上巻)-基礎・臨床研究の最新動向-
日本臨牀 2018
Author:川岸裕幸; 三河隆太; 杉本昌隆


Articles
Cytokine receptor gp130 promotes postnatal proliferation of cardiomyocytes required for the normal functional development of the heart
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY,323(1):H103-H120 2022(Jul.)
Author:Kawagishi, Hiroyuki; Nakada, Tsutomu; Numaga-Tomita, Takuro; Larranaga, Maite; Guo, Ang; Song, Long-Sheng; Yamada, Mitsuhiko;
Keywords:cardiomyocyte; gp130; interleukin-6; neonate; proliferation;


Cytokine receptor gp130 promotes postnatal proliferation of cardiomyocytes required for the normal functional development of the heart
American Journal of Physiology-Heart and Circulatory Physiology 2022(May 20)
Author:Hiroyuki Kawagishi; Tsutomu Nakada; Takuro Numaga-Tomita; Maite Larrañaga; Ang Guo; Long-Sheng Song; Mitsuhiko Yamada
Abstract:Mammalian ventricular cardiomyocytes are premature at birth and exhibit substantial phenotypic changes before weaning. Mouse ventricular myocytes undergo cell division several times after birth; however, the regulatory mechanisms and roles of cardiomyocyte division in postnatal heart development remain unclear. Here, we investigated the physiological role of gp130, the main subunit of multifunctional receptors for the IL-6 family of cytokines, in postnatal cardiomyocyte proliferation. Pharmacological inhibition of gp130 within the first month after birth induced significant systolic dysfunction of the left ventricle in mice. Consistently, mice with postnatal cardiomyocyte-specific gp130 depletion exhibited impaired left ventricular contractility compared to control mice. In these mice, cardiomyocytes exhibited a moderately decreased size and dramatically inhibited proliferation in the left ventricle but not in the right ventricle. Stereological analysis revealed that this change significantly decreased the number of cardiomyocytes in the left ventricle. Furthermore, IL-6 was mainly responsible for promoting ventricular cardiomyocyte proliferation by activating the JAK/STAT3 pathway. Taken together, the IL-6/gp130/JAK/STAT3 axis plays a crucial role in the physiological postnatal proliferation and hypertrophy of left ventricular cardiomyocytes to ensure normal cardiac functional development.


Adrenomedullin-RAMP2 and -RAMP3 Systems Regulate Cardiac Homeostasis during Cardiovascular Stress
Endocrinology,162(3) 2021(Mar. 01)
Author:Nanqi Cui; Takayuki Sakurai; Akiko Kamiyoshi; Yuka Ichikawa-Shindo; Hisaka Kawate; Megumu Tanaka; Masaaki Tanaka; Yangxuan Wei; Shinji Kakihara; Yunlu Zhao; Kohsuke Aruga; Hiroyuki Kawagishi; Tsutomu Nakada; Mitsuhiko Yamada; Takayuki Shindo
Abstract:Abstract Adrenomedullin (AM) is a peptide hormone with multiple physiological functions, which are regulated by its receptor activity–modifying proteins, RAMP2 and RAMP3. We previously reported that AM or RAMP2 knockout (KO) (AM–/–, RAMP2–/–) is embryonically lethal in mice, whereas RAMP3–/– mice are apparently normal. AM, RAMP2, and RAMP3 are all highly expressed in the heart; however, their functions there are not fully understood. Here, we analyzed the pathophysiological functions of the AM-RAMP2 and AM-RAMP3 systems in hearts subjected to cardiovascular stress. Cardiomyocyte-specific RAMP2–/– (C-RAMP2–/–) and RAMP3–/– showed no apparent heart failure at base line. After 1 week of transverse aortic constriction (TAC), however, C-RAMP2–/– exhibited significant cardiac hypertrophy, decreased ejection fraction, and increased fibrosis compared with wild-type mice. Both dP/dtmax and dP/dtmin were significantly reduced in C-RAMP2–/–, indicating reduced ventricular contractility and relaxation. Exposing C-RAMP2–/– cardiomyocytes to isoproterenol enhanced their hypertrophy and oxidative stress compared with wild-type cells. C-RAMP2–/– cardiomyocytes also contained fewer viable mitochondria and showed reduced mitochondrial membrane potential and respiratory capacity. RAMP3–/– also showed reduced systolic function and enhanced fibrosis after TAC, but those only became apparent after 4 weeks. A reduction in cardiac lymphatic vessels was the characteristic feature in RAMP3–/–. These observations indicate the AM-RAMP2 system is necessary for early adaptation to cardiovascular stress through regulation of cardiac mitochondria. AM-RAMP3 is necessary for later adaptation through regulation of lymphatic vessels. The AM-RAMP2 and AM-RAMP3 systems thus play separate critical roles in the maintenance of cardiovascular homeostasis against cardiovascular stress.


β-Arrestin-Biased AT1 Agonist TRV027 Causes a Neonatal-Specific Sustained Positive Inotropic Effect Without Increasing Heart Rate.
JACC. Basic to translational science,5(11):1057-1069 2020(Nov.)
Author:Toshihide Kashihara; Hiroyuki Kawagishi; Tsutomu Nakada; Takuro Numaga-Tomita; Shin Kadota; Elena E Wolf; Cheng-Kun Du; Yuji Shiba; Sachio Morimoto; Mitsuhiko Yamada
Abstract:The treatment of pediatric heart failure is a long-standing unmet medical need. Angiotensin II supports mammalian perinatal circulation by activating cardiac L-type Ca2+ channels through angiotensin type 1 receptor (AT1R) and β-arrestin. TRV027, a β-arrestin-biased AT1R agonist, that has been reported to be safe but not effective for adult patients with heart failure, activates the AT1R/β-arrestin pathway. We found that TRV027 evokes a long-acting positive inotropic effect specifically on immature cardiac myocytes through the AT1R/β-arrestin/L-type Ca2+ channel pathway with minimum effect on heart rate, oxygen consumption, reactive oxygen species production, and aldosterone secretion. Thus, TRV027 could be utilized as a valuable drug specific for pediatric heart failure.


Acetylation-mediated remodeling of the nucleolus regulates cellular acetyl-CoA responses.
PLoS biology,18(11):e3000981 2020(Nov.)
Author:Ryan Houston; Shiori Sekine; Michael J Calderon; Fayaz Seifuddin; Guanghui Wang; Hiroyuki Kawagishi; Daniela A Malide; Yuesheng Li; Marjan Gucek; Mehdi Pirooznia; Alissa J Nelson; Matthew P Stokes; Jacob Stewart-Ornstein; Steven J Mullett; Stacy G Wendell; Simon C Watkins; Toren Finkel; Yusuke Sekine
Abstract:The metabolite acetyl-coenzyme A (acetyl-CoA) serves as an essential element for a wide range of cellular functions including adenosine triphosphate (ATP) production, lipid synthesis, and protein acetylation. Intracellular acetyl-CoA concentrations are associated with nutrient availability, but the mechanisms by which a cell responds to fluctuations in acetyl-CoA levels remain elusive. Here, we generate a cell system to selectively manipulate the nucleo-cytoplasmic levels of acetyl-CoA using clustered regularly interspaced short palindromic repeat (CRISPR)-mediated gene editing and acetate supplementation of the culture media. Using this system and quantitative omics analyses, we demonstrate that acetyl-CoA depletion alters the integrity of the nucleolus, impairing ribosomal RNA synthesis and evoking the ribosomal protein-dependent activation of p53. This nucleolar remodeling appears to be mediated through the class IIa histone deacetylases (HDACs). Our findings highlight acetylation-mediated control of the nucleolus as an important hub linking acetyl-CoA fluctuations to cellular stress responses.


Macrophage fatty acid oxidation inhibits atherosclerosis progression.
Journal of molecular and cellular cardiology 2019(Jan.)
Author:Nomura M; Liu J; Yu ZX; Yamazaki T; Yan Y; Kawagishi H; Rovira II; Liu C; Wolfgang MJ; Mukouyama YS; Finkel T


Increase in phospholamban content in mouse skeletal muscle after denervation.
Journal of muscle research and cell motility,39(5-6):163-173 2018(Dec.)
Author:Komatsu M; Nakada T; Kawagishi H; Kato H; Yamada M


Prostanoid EP4 receptor-mediated augmentation of Ih currents in Aβ dorsal root ganglion neurons underlies neuropathic pain.
The Journal of pharmacology and experimental therapeutics,368(1):50-58 2018(Nov.)
Author:Zhang H; Kashihara T; Nakada T; Tanaka S; Ishida K; Fuseya S; Kawagishi H; Kiyosawa K; Kawamata M; Yamada M


Sonic hedgehog signaling regulates the mammalian cardiac regenerative response.
Journal of molecular and cellular cardiology,123:180-184 2018(Oct.)
Author:Kawagishi H; Xiong J; Rovira II; Pan H; Yan Y; Fleischmann BK; Yamada M; Finkel T


A Metabolic Basis for Endothelial-to-Mesenchymal Transition.
Molecular cell,69(4):689-698.e7 2018(Feb.)
Author:Xiong J; Kawagishi H; Yan Y; Liu J; Wells QS; Edmunds LR; Fergusson MM; Yu ZX; Rovira II; Brittain EL; Wolfgang MJ; Jurczak MJ; Fessel JP; Finkel T


Elimination of p19ARF-expressing cells enhances pulmonary function in mice.
JCI insight,1(12):e87732 2016(Aug. 04)
Author:Michihiro Hashimoto; Azusa Asai; Hiroyuki Kawagishi; Ryuta Mikawa; Yuji Iwashita; Kazuki Kanayama; Kazushi Sugimoto; Tadashi Sato; Mitsuo Maruyama; Masataka Sugimoto
Abstract:Senescent cells accumulate in many tissues as animals age and are considered to underlie several aging-associated pathologies. The tumor suppressors p19ARF and p16INK4a, both of which are encoded in the CDKN2A locus, play critical roles in inducing and maintaining permanent cell cycle arrest during cellular senescence. Although the elimination of p16INK4a-expressing cells extends the life span of the mouse, it is unclear whether tissue function is restored by the elimination of senescent cells in aged animals and whether and how p19ARF contributes to tissue aging. The aging-associated decline in lung function is characterized by an increase in compliance as well as pathogenic susceptibility to pulmonary diseases. We herein demonstrated that pulmonary function in 12-month-old mice was reversibly restored by the elimination of p19ARF-expressing cells. The ablation of p19ARF-expressing cells using a toxin receptor-mediated cell knockout system ameliorated aging-associated lung hypofunction. Furthermore, the aging-associated gene expression profile was reversed after the elimination of p19ARF. Our results indicate that the aging-associated decline in lung function was, at least partly, attributed to p19ARF and was recovered by eliminating p19ARF-expressing cells.


Loss of HuR leads to senescence-like cytokine induction in rodent fibroblasts by activating NF-kappa B
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS,1840(10):3079-3087 2014(Oct.)
Author:Michihiro Hashimoto; Takayuki Tsugawa; Hiroyuki Kawagishi; Azusa Asai; Masataka Sugimoto
Abstract:Background: HuR (human antigen R) is a ubiquitously expressed member of the Hu/ELAV family of proteins that is involved in diverse biological processes. HuR has also been shown to play an important role in cell cycle arrest during replicative senescence in both human and mouse cells. Senescent cells not only halt their proliferation, but also activate the secretion of proinflammatory cytokines. A persistent DNA damage response is essential for the senescence-associated secretory phenotype (SASP), and increasing evidence has suggested that the SASP is associated with malignancy. Methods: Senescence-associated phenotypes were analyzed in MEFs and other cell line in which HuR expression is inhibited by sh-RNA-mediated knockdown. Results: RNAi-mediated HuR inhibition resulted in an increase in SASP-related cytokines. The induction of SASP factors did not depend on ARF-p53 pathway-mediated cell cycle arrest, but required NF-kappa B activity. In the absence of HuR, cells were defective in the DNA-damage response, and single strand DNA breaks accumulated, which may have caused the activation of NF-kappa B and subsequent cytokine induction. Conclusions: In the absence of HuR, cells exhibit multiple senescence-associated phenotypes. Our findings suggest that HuR regulates not only the replicative lifespan, but also the expression of SASP-related cytokines in mouse fibroblasts. General significance: RNA-binding protein HuR protects cells from undergoing senescence. Senescence-associated phenotypes are accelerated in HuR-deficient cells. (C) 2014 Elsevier B.V. All rights reserved.


HuR Maintains a Replicative Life Span by Repressing the ARF Tumor Suppressor
MOLECULAR AND CELLULAR BIOLOGY,33(10):1886-1900 2013(May)
Author:Hiroyuki Kawagishi; Michihiro Hashimoto; Hideaki Nakamura; Takayuki Tsugawa; Atsushi Watanabe; Dimitris L. Kontoyiannis; Masataka Sugimoto
Abstract:p19(ARF) plays an essential role in the senescence of mouse cells, and its expression is lost by methylation or deletion of the ARF locus; otherwise, p53 is inactivated to bypass senescence. ARF expression is tightly regulated, but little is known about its posttranscriptional regulation. Here, we show that an RNA-binding protein, HuR (human antigen R), represses ARF mRNA translation, thereby maintaining the replicative life span of mouse embryonic fibroblasts (MEFs). Loss of HuR results in premature senescence, with concomitant increases in p19(ARF) but not p16(Ink4a) levels, and this senescence is not observed in ARF-null MEFs that retain an intact Ink4a locus. HuR depletion does not alter ARF transcription or stability but enhances ribosome association with ARF mRNA. Under these conditions, ARF mRNA accumulates in nucleoli, where it associates with nucleolin. Furthermore, adipose-specific deletion of the HuR gene results in increased p19(ARF) expression in aged animals, which is accompanied by decreased insulin sensitivity. Together, our findings demonstrate that p19(ARF) is also regulated at the translational level, and this translational regulation restrains the cellular life span and tissue functions in vivo.


Cooperative Role of the RNA-Binding Proteins Hzf and HuR in p53 Activation
MOLECULAR AND CELLULAR BIOLOGY,31(10):1997-2009 2011(May)
Author:Hideaki Nakamura; Hiroyuki Kawagishi; Atsushi Watanabe; Kazushi Sugimoto; Mitsuo Maruyama; Masataka Sugimoto
Abstract:The RNA-binding protein Hzf (hematopoietic zinc finger) plays important roles in mRNA translation in cerebellar Purkinje cells and adipocytes. We along with others have reported that the expression of the Hzf gene is transcriptionally regulated by the p53 tumor suppressor protein. We show here that Hzf regulates p53 expression in cooperation with HuR. Hzf and HuR independently interact with the 3' untranslated region (UTR) of p53 mRNA, which facilitates the cytoplasmic localization of p53 mRNA in the presence of the ARF tumor suppressor protein. In the absence of Hzf and HuR, p53 induction by p19(ARF) is significantly attenuated, and the cells consequently acquire resistance to p19(ARF). Thus, these findings demonstrate that in addition to Mdm2 inhibition, p19(ARF) increases the concentration of p53 through posttranscriptional control of p53 mRNA and suggest critical roles for the RNA-binding proteins Hzf and HuR in p53 induction.


ARF suppresses tumor angiogenesis through translational control of VEGFA mRNA
Cancer Research,70(11):4749-4758 2010(Jun. 01)
Author:Hiroyuki Kawagishi; Hideaki Nakamura; Mitsuo Maruyama; Shuki Mizutani; Kazushi Sugimoto; Masatoshi Takagi; Masataka Sugimoto
Abstract:Vascular endothelial growth factor A (VEGFA) is a specific mitogen for vascular endothelial cells that plays a critical role in cancer neoangiogenesis. Here, we report that the nucleolar tumor suppressor p19ARF suppresses VEGFA expression, acting at the level of mRNA translation without affecting the transcription of the VEGFA gene. Translational repression of VEGFA mRNA by p19ARF does not require p53, a major target of the ARF tumor suppressor pathway, but instead correlates with binding to nucleophosmin/B23. Maintaining VEGFA expression relies on nucleophosmin/B23, and downregulating this protein by RNAi or p19ARF leads to translational repression of VEGFA. p19ARF inhibits VEGFA-dependent tumor angiogenesis in nude mice. Additionally, p14ARF expression and microvessel density are inversely correlated in human colon carcinomas. Taken together, our results define a mechanism by which the ARF tumor suppressor targets the translational repression of specific oncogenes during neoplastic transformation. ©2010 AACR.


Hzf regulates adipogenesis through translational control of C/EBPα
EMBO Journal,27(10):1481-1490 2008(May 21)
Author:Hiroyuki Kawagishi; Takeshi Wakoh; Hatsume Uno; Mitsuo Maruyama; Ayako Moriya; Satoru Morikawa; Hideyuki Okano; Charles J. Sherr; Masatoshi Takagi; Masataka Sugimoto
Abstract:Adipocyte differentiation requires a well-defined programme of gene expression in which the transcription factor C/EBPα (CCAAT/enhancer- binding protein) has a central function. Here, we show that Hzf (haematopoietic zinc-finger), a previously identified p53 transcriptional target, regulates C/EBPα expression. Hzf is induced during differentiation of preadipocyte cell lines, and its suppression by short hairpin RNA disrupts adipogenesis. In Hzf's absence, expression of C/EBPα is severely impaired because of reduced translation of its mRNA. Hzf physically interacts with the 3′ untranslated region of C/EBPα mRNA to enhance its translation. Taken together, these findings underscore a critical role of Hzf in the adipogenesis regulatory cascade. © 2008 European Molecular Biology Organization | All Rights Reserved.


Presentations
In-vitro and pharmacovigilance assessments of cardiotoxicity of VEGFR-tyrosine kinase inhibitors
第97回日本薬理学年会 2023(Dec. 16)
Presenter:川岸裕幸; 柳田翔太; 安慶名結衣; 諫田泰成


Mechanisms underlying the efficacy and safety of β-arrestin-biased AT1 agonists as therapeutics for neonatal and infantile heart failure
第97回日本薬理学会年会 2023(Dec. 16)
Presenter:川岸裕幸; 中島岳郎; 松岡大輔; 中田勉; 冨田拓郎; 諫田泰成; 山田充彦


Assessment of Cardiac Contractility Using Aligned Human iPS Cell-Derived Cardiomyocytes
2023 Safety Pharmacology Society (SPS) ANNUAL MEETING 2023(Sep. 19)
Presenter:Hiroyuki Kawagishi; Ayano Satsuka; Shota Yanagita; Naoya Hirata; Yasunari Kanda


液性因子による新生児期特有の生理作用と その制御機構の探索
第46回日本基礎老化学会大会 2023(Jun. 17)
Presenter:川岸裕幸


βアレスチンバイアスAT1Rアゴニストはヒト先天性拡張心筋症マウスの離乳前生命予後を改善する
第32回日本循環薬理学会 2023(Jan. 27)
Presenter:川岸 裕幸; 冨田(沼賀) 拓郎; 中田 勉; 山田 充彦


幼若心筋細胞におけるリガンド特異的gp130受容体シグナルの意義
2022年 筋生理の集い 2022(Dec. 10)
Presenter:川岸裕幸; 山田充彦


β-arrestin-biased AT1R agonist improves health- and lifespan in mice with congenital dilated cardiomyopathy
第96回日本薬理学会年会 2022(Nov. 30)
Presenter:Hiroyuki Kawagishi; Risa Ramadhiani; Naoto Minamino; Takuro Tomita-Numaga; Tsutomu Nakada; Noriaki Emoto; Mitsuhiko Yamada


インターロイキン-6/gp130 経路による出生後心筋細胞の分裂制御と心臓の機能的発達における意義
生理研研究会 比較統合生理学的観点からの循環生理の解析 2022(Oct. 13)
Presenter:川岸 裕幸


出生後の心筋細胞分裂におけるインターロイキン-6/gp130シグナル経路の役割
第51回日本心脈管作動物質学会 2022(Jul. 30)
Presenter:川岸裕幸, 中田勉, 冨田(沼賀)拓郎, 山田充彦


Interleukin-6/gp130 signaling controls postnatal proliferation of mouse ventricular cardiomyocytes
第45回日本基礎老化学会大会 2022(Jul. 27)
Presenter:KAWAGISHI Hiroyuki; NAKADA Tsutomu; NUMAGA-TOMITA Takuro; YAMADA Mitsuhiko


インターロイキン-6/gp130経路による出生後心室筋細胞の分裂制御と心臓
第146回日本薬理学会関東部会 2022(Jun. 18)
Presenter:川岸裕幸, 中田勉, 冨田(沼賀)拓郎, 山田充彦


Rapid increase in aerobic glycolysis in neonatal mouse ventricular cardiomyocytes in response to acute β-adrenergic stimulation
第95回日本薬理学会年会 2022(Mar. 09)
Presenter:Hiroyuki Kawagishi; Tsutomu Nakada; Takuro Tomita-Numaga; Mitsuhiko Yamada


AT1アンジオテンシン受容体の新規生理特性を利用した 小児心不全治療法の創出
第31回日本循環薬理学会 2021(Dec. 03)
Presenter:川岸 裕幸; 冨田(沼賀) 拓郎; 中田 勉; 松岡 大輔; 山田 充彦


Physiological role of gp130 in postnatal proliferation of cardiomyocytes and functional development of heart
生理研研究会 2021(Nov. 18)
Presenter:川岸裕幸; 中田勉; 冨田(沼賀)拓郎; Maite Larrañaga; 山田充彦


βアレスチンバイアス性アンジオテンシンII 1型受容体アゴニストによる 新たな小児心不全治療戦略の創生
第50回日本心脈管作動物質学会 2021(Jul. 16)
Presenter:川岸 裕幸; 冨田(沼賀) 拓郎; 中田 勉; 松岡 大輔; 柴 祐司; 森本 幸生; 山田 充彦


Postnatal loss of gp130 caused impaired physiological proliferation of mouse cardiomyocytes
第44回 日本基礎老化学会大会 2021(Jun. 12)
Presenter:KAWAGISHI Hiroyuki; NAKADA Tsutomu; NUMAGA-TOMITA Takuro; YAMADA Mitsuhiko


AT1アンジオテンシン受容体の生理作用を利用した新規乳幼児心不全治療薬の開発
第144回日本薬理学会関東部会 2021(Jun. 05)
Presenter:川岸裕幸; 冨田(沼賀)拓郎; 中田勉; 柴裕司; 森本幸生; 山田充彦


A novel way of modification of AT1 angiotensin receptors to alleviate pediatric heart failure
第94回日本薬理学会年会 2021(Mar. 09)
Presenter:Hiroyuki KAWAGISHI; Takuro NUMAGA-TOMITA; Tsutomu NAKADA; Toshihide KASHIHARA; Mitsuhiko YAMADA


Postnatal loss of gp130 caused impaired cardiac contractility accompanied by inhibition of physiological proliferation of cardiomyocytes
心血管国際研究集会2020 2020(Dec. 25)
Presenter:Hiroyuki Kawagishi; Tsutomu Nakada; Takuro Numaga-Tomita; Mitsuhiko Yamada


アンジオテンシンII 1型受容体ーβアレスチン経路を活性化する小児心不全治療薬の開発
第30回日本循環薬理学会 2020(Nov. 27)
Presenter:川岸裕幸; 柏原俊英; 冨田(沼賀)拓郎; 中田勉; 山田充彦


新たな方法でAT1受容体を利用した小児心不全治療薬の開発
第143回日本薬理学会関東部会 2020(Oct. 24)
Presenter:川岸裕幸


βアレスチンバイアスアンジオテンシン1型受容体アゴニストは、新生児特有の持続性陽性変力作用を示す
第142回日本薬理学会関東部会 2020(Jun. 06)


新生児マウスにおける、gp130受容体を介した心筋細胞の発達機構
2019年 筋生理の集い 2019(Dec. 21)


Physiological role of gp130 receptor in newborn mouse cardiomyocyte development
'MIRACLES' in Cardiovascular Physiology ~Metabolism, Interactions, Regulation, Application, Chemical Biology, Longevity, Exercise and Signaling~ 2019(Dec. 06)


βアレスチンバイアス アンジオテンシン1型受容体アゴニストは、 新生児マウス心臓において持続的な陽性変力作用を示す
第29回日本循環薬理学会 2019(Nov. 29)


βアレスチンバイアスAT1受容体アゴニストは、新生児マウス心臓において持続的な陽性変力作用を示す
第21回応用薬理シンポジウム 2019(Sep. 21)


マウス心筋細胞の生下後の機能的最終分化の分子メカニズムの解析
第140回日本薬理学会関東部会 2019(Jul. 09)


Sonic Hedgehog signaling regulates the mammalian cardiac regenerative response
9th FAOPS 2019(Mar. 30)


Factors inducing final cardiomyocyte maturation in newborn mice
第92回日本薬理学会年会 2019(Mar. 16)


新生児マウスの心臓における、 β-アレスチン選択的アンジオテンシン受容体アゴニストによる陽性変力作用
第28回日本循環薬理学会 2018(Dec. 07)
Presenter:川岸裕幸


新生児マウスの心臓におけるアンジオテンシンII 1型受容体-βアレスチン経路による陽性変力作用
第139回日本薬理学会関東部会 2018(Oct. 20)
Presenter:川岸裕幸


Sonic Hedgehog signaling regulates the mammalian cardiac regenerative response
18th World Congress of Basic and Clinical Pharmacology 2018(Jul.)
Presenter:Hiroyuki KawagishiHiroyuki Kawagishi; Jianhua Xiong; Toren Finkel


Sonic Hedgehog signaling regulates the mammalian cardiac regenerative response
ConBio2017 2017(Dec.)
Presenter:Hiroyuki Kawagishi; Jianhua Xiong; Toren Finkel


Role of sonic hedgehog signaling in heart regeneration.
Leducq annual meeting 2017(Feb.)
Presenter:Hiroyuki Kawagishi


Role of sonic hedgehog signaling in mammalian cardiac regeneration
国立長寿医療研究センター NCGGセミナー 2016(Feb.)
Presenter:Hiroyuki KAWAGISHI


Role of sonic hedgehog signaling in heart regeneration
Leducq annual meeting 2016(Jan.)
Presenter:Hiroyuki Kawagishi


Role of mitochondrial protein CPT1A in sonic hedgehog signaling
JSPS-NIH meeting 2014(Oct.)
Presenter:Hiroyuki Kawagishi; Jianhua Xiong; Toren Finkel


HuR maintains replicative lifespan by suppressing ARF tumor suppressor.
名古屋大学GCOEリトリート 2012(Mar.)
Presenter:Hiroyuki Kawagishi; Hideaki Nakamura; Takayuki Tsugawa; Masataka Sugimoto


HuR maintains replicative lifespan by repressing ARF tumor suppressor.
第34回分子生物学会年会 2011(Dec.)
Presenter:Hiroyuki Kawagishi; Hideaki Nakamura; Takayuki Tsugawa; Masataka Sugimoto


RNA-binding protein HuR suppresses cellular senescence by repressing the translation of ARF mRNA.
Mechanisms & Models of Cancer Symposium in SALK instate 2011(Aug.)
Presenter:Hiroyuki Kawagishi; Masataka Sugimoto


HuR maintains replicative lifespan by repressing ARF tumor suppressor.
FANTASY 2011(Feb.)
Presenter:Hiroyuki Kawagishi


ARF tumor suppressor regulates tumor angiogenesis through translational control of VEGFA mRNA.
第32回分子生物学会年会 2009(Dec.)
Presenter:Kawagishi H; Maruyama M; Takagi M; Sugimoto M


ARF tumor suppressor inhibits the translation of VEGF mRNA.
FANTASY 2008(Jan.)
Presenter:Hiroyuki Kawagishi


ARF tumor suppressor inhibits the translation of VEGF mRNA.
第30回日本分子生物学会年会・第80回日本生化学会大会合同大会 2007(Dec.)
Presenter:川岸裕幸; 高木正稔; 杉本昌隆


ARF tumor suppressor regulates the translation of VEGF mRNA.
第9回日本RNA学会年会 2007(Aug.)
Presenter:川岸裕幸; 丸山光生; 高木正稔; 杉本昌隆


MISC
新生児マウス心臓の機能的発達におけるサイトカイン受容体gp130の役割
信州医学雑誌 2022
Author:川岸裕幸; 山田充彦


βアレスチンバイアス性アンジオテンシンII 1型受容体アゴニストによる新たな小児心不全治療戦略の創生.
血管 2022
Author:川岸裕幸; 山田充彦


βアレスチンバイアスAT1受容体アゴニストは新しい乳幼児心不全治療薬の有力候補である。
医学のあゆみ,276(12):1137-1138 2021(Mar.)
Author:川岸裕幸; 山田充彦


A novel way of modification of AT1 angiotensin receptors to alleviate neonatal and infantile heart failure
Folia Pharmacologica Japonica,156(6):351-354 2021
Author:Hiroyuki Kawagishi; Mitsuhiko Yamada


Unraveling the Truth About Antioxidants: ROS and disease: finding the right balance
Nature Medicine,20(7):711-713 2014(Jul.)
Author:Hiroyuki Kawagishi; Toren Finkel


癌抑制・細胞老化因子ARFが引き起こす血管新生抑制及び疾患との関わり
基礎老化研究,34(3):19-21 2010
Author:川岸 裕幸; 丸山 光生; 高木 正稔; 杉本 昌隆

Research Grants
Grants‐in‐aid for Scientific Research(Research Representative)
アデノ随伴ウイルスを用いた心臓特異的遺伝子抑制による心筋細胞成熟化因子の同定 , 若手研究
2018 - 2019 , マウス個体を用いた心筋細胞の成熟化因子の探索 , 研究活動スタート支援
- 2023 , 新生児低血糖症における心臓の未知の生理的役割とその分子機構の解明 , 基盤研究(C)

Scholarship donation
2021 , 低出生体重児の子宮外後腎分化誘導法の開発
Developmental Origins of Health and DiseaseとしてのAT1受容体による腎脈管・血管形成誘導メカニズムの解明
AT1アンジオテンシン受容体-βアレスチン系を活性化する新規小児心不全治療薬開発
βアレスチン選択的アンジオテンシン受容体アゴニストによる新規小児心不全治療薬の開発
新生児期に起こる心筋細胞の分裂増殖の分子メカニズム
新生児期のアンジオテンシンIIによる副腎髄質カテコラミン興奮分泌機構の制御
抗腫瘍薬治療による晩期心機能障害の発生機序の解明
マウス心筋細胞の機能的最終分化におけるgp130シグナルの役割
マウス個体を用いた心筋細胞成熟化メカニズムの解明