Core Program members: Motoaki Sano

Core Program members | Program members | Research Assistants and Fellows

Motoaki Sano

Associate Professor


Backgrounds

1992-94: Resident in Internal Medicine, Keio University School of Medicine, Tokyo, Japan
1994-95: Medical Staff in Internal Medicine, Mito Red-Cross Hospital, Mito, Japan
1995-96: Medical Staff in Internal Medicine, Keiyu Hospital, Yokohama, Japan
1996-2000: Clinical Cardiology Fellow, Keio University School of Medicine, Tokyo, Japan
1996-2000: Postgraduate (ph. D.) course in Medicine, Keio University, Tokyo, Japan
2000-2004: Postdoctoral Fellow, Department of Medicine, Section of Cardiology, Baylor College of Medicine (Dr. Michael D. Schneider)
2004-2005: Assistant professor, Department of Medicine, Section of Cardiology, Baylor College of Medicine
2005-2006: Assistant professor, Department of Regenerative Medicine and Advanced Cardiac Therapeutics, Keio University School of Medicine, Tokyo,Japan
2006-: Associate professor, Department of Regenerative Medicine and Advanced Cardiac Therapeutics, Keio University School of Medicine, Tokyo,Japan
2006-: Precursory Research for Embryonic Science and Technology (PRESTO), Japan Science and Technology Agency, Saitama, Japan (hold a post concurrently)

Awards and Honors

2000: Japan Heart Foundation and the Bayer Yakuhin Research Grant Abroad
2002: Baylor College of Medicine Section of Cardiology, Recognition of Best Basic Research
2003: Heart Failure Society America, Jay N. Cohn New Investigator Award (Basic Science)
2003: Council on Basic Cardiovascular Sciences, Melvin L. Marcus Young Investigator Award in Cardiovascular Science
2005: International Society for Hear Research (North America), Young Investigator Award
2005: Keio Sanshikai Award
2007: International Society for Hear Research (Japan), Young Investigator Award

Research Overview

The heart failure increases dramatically with age. Heart is a postmitotic organ, therefore, myocardial aging, such as under repeated oxidative stress, is characterized by a loss of specialized cellular functions. The final avenue of exploration in understanding cellular function is the metabolites that occur as the end products of cellular metabolism (metabolome). The change of cardiac metabolites, along with improper degradation and synthesis of cellular proteins, may lead to myocardial aging. Through the comprehensive analysis of metabolome and transcriptome, we try to understand the cellular and molecular mechanism of heart failure, especially in the context of myocardial aging.

Major Publications

Pan J, Fukuda K, Kodama H, Makino S, Takahashi T, Sano M, Hori S, Ogawa S. Role of angiotensin II in activation of the JAK/STAT pathway induced by acute pressure overload in the rat heart. Circ Res. 81, 611-7 (1997)
Pan J, Fukuda K, Kodama H, Sano M, Takahashi T, Makino S, Kato T, Manabe T, Hori S, Ogawa S. Involvement of gp130-mediated signaling in pressure overload-induced activation of the JAK/STAT pathway in rodent heart. Heart Vessels.;13, 199-208 (1998)
Kodama H, Fukuda K, Pan J, Makino S, Sano M, Takahashi T, Hori S, Ogawa S. Biphasic activation of the JAK/STAT pathway by angiotensin II in rat cardiomyocytes. Circ Res. 82, 244-50 (1998)
Makino S, Fukuda K, Miyoshi S, Konishi F, Kodama H, Pan J, Sano M, Takahashi T, Hori S, Abe H, Hata J, Umezawa A, Ogawa S. Cardiomyocytes can be generated from marrow stromal cells in vitro. J Clin Invest. 103, 697-705. (1999)
Pan J, Fukuda K, Saito M, Matsuzaki J, Kodama H, Sano M, Takahashi T, Kato T, Ogawa S. Mechanical stretch activates the JAK/STAT pathway in rat cardiomyocytes. Circ Res. 84, 1127-36 (1999)
Takahashi T, Fukuda K, Pan J, Kodama H, Sano M, Makino S, Kato T, Manabe T, Ogawa S. Characterization of insulin-like growth factor-1-induced activation of the JAK/STAT pathway in rat cardiomyocytes.Circ Res. 85, 884-91 (1999)
Kodama H, Fukuda K, Pan J, Sano M, Takahashi T, Kato T, Makino S, Manabe T, Murata M, Ogawa S. Significance of ERK cascade compared with JAK/STAT and PI3-K pathway in gp130-mediated cardiac hypertrophy. Am J Physiol Heart Circ Physiol. 279, H1635-44 (2000)
Sano M, Fukuda K, Kodama H, Pan J, Saito M, Matsuzaki J, Takahashi T, Makino S, Kato T, Ogawa S. Interleukin-6 family of cytokines mediate angiotensin II-induced cardiac hypertrophy in rodent cardiomyocytes. J Biol Chem 275, 29717-23 (2000)
Sano M, Fukuda K, Kodama H, Takahashi T, Kato T, Hakuno D, Sato T, Manabe T, Tahara S, Ogawa S. Autocrine/paracrine secretion of IL-6 family cytokines causes angiotensin II-induceddelayed STAT3 activation. Biochem Biophys Res Commun. 269, 798-802. (2000)
Sano M, Kato T, Miyoshi S, Sato T, Hakuno D, Ishida H, Kinoshita-Nakazawa H, Fukuda K, Ogawa S. Calmodulin kinases II and IV and calcineurin are involved in leukemia inhibitory factor-induced cardiac hypertrophy in rats. Circ Res. 87, 937-45 (2000)
Sano M, Fukuda K, Sato T, Kawaguchi H, Suematsu M, Matsuda S, Koyasu S, Matsui H, Yamauchi-Takihara K, Harada M, Saito Y, Ogawa S. ERK and p38 MAPK, but not NF-kappaB, are critically involved in reactive oxygen species-mediated induction of IL-6 by angiotensin II in cardiac fibroblasts. Circ Res. 89, 661-9 (2001)
Kodama H, Fukuda K, Takahashi T, Sano M, Kato T, Tahara S, Hakuno D, Sato T, Manabe T, Konishi F, Ogawa S. Role of EGF receptor and Pyk2 in endothelin-1-induced ERK activation in rat cardiomyocytes. J Mol Cell Cardiol. 34, 139-50 (2002)
Sano M, Schneider MD. Still stressed out but doing fine: normalization of wall stress is superfluous to maintaining cardiac function in chronic pressure overload. Circulation. 105, 8-10 (2002)
Sano M, Abdellatif M, Oh H, Xie M, Bagella L, Giordano A, Michael LH, DeMayo FJ, Schneider MD. (2002) Activation and function of cyclin T/Cdk9 (positive transcription elongation factor-b) in cardiac muscle cell hypertrophy. Nature Medicine, Nat Med. 8, 1310-7 (2002)
Oh H, Wang SC, Prahash A, Sano M, Moravec CS, Taffet GE, Michaels LH, Youker KA, Entman ML, Schneider MD. Telomere attrition and chk2 activation in human heart failure. Proc.Natl.Acad.Sci.U.S,A. 100, 5378-83.
Nakamura T, Sano M, Songyang Z, Schneider MD. A Wnt- and b-catenin-dependent pathway for mammalian cardiac myogenesis. Proc.Natl.Acad.Sci.U.S.A.100, 5834-9.
Sano M, Schneider MD. Cyclins that don't cycle: Cyclin T/Cyclin-dependent kinase-9 determines cardiac muscle cell size. Cell cycle. 2, 99-104 (2003)
Kulkarni PA, Sano M, Schneider MD. Phosphorylation of RNA polymerase II in cardiac hypertrophy: cell enlargement signals converge on cyclin T/Cdk9.Recent Prog Horm Res. 59:125-39. (2004)
Sano M, Wang SC, Shirai M, Scaglia F, Xie M, Sakai S, Tanaka T, Kulkarni PA, Barger PM, Youker KA, Taffet GE, Hamamori Y, Michael LH, Craigen WJ, Schneider MD.Activation of cardiac Cdk9 represses PGC-1 and confers a predisposition to heart failure.
EMBO J. 23:3559-69 (2004)
Sano M, Schneider MD. Cyclin-dependent kinase-9: an RNAPII kinase at the nexus of cardiac growth and death cascades. Circ Res. 95:867-76. (2004)
Ieda M, Kanazawa H, Ieda Y, Kimura K, Matsumura K, Tomita Y, Yagi T, Onizuka T, Shimoji K, Ogawa S, Makino S, Sano M, Fukuda K. Nerve growth factor is critical for cardiac sensory innervation and rescues neuropathy in diabetic hearts. Circulation. 114:2351-63. (2006)
Sano, M., Y. Izumi, K. Helenius, M. Asakura, D.J. Rossi, M. Xie, G. Taffet, L. Hu, R.G. Pautler, C.R. Wilson, S. Boudina, E.D. Abel, H. Taegtmeyer, F. Scaglia, B.H. Graham, A. Kralli, N. Shimizu, H. Tanaka, T.P. Makela, and M.D. Schneider. Menage-a-Trois 1 Is Critical for the Transcriptional Function of PPARgamma Coactivator 1. Cell Metab. 5:129-42. (2007).
Liu Y, Asakura M, Inoue H, Nakamura T, Sano M, Niu Z, Chen M, Schwartz RJ, Schneider MD. Sox17 is essential for the specification of cardiac mesoderm in embryonic stem cells. Proc Natl Acad Sci U S A. 104:3859-64 (2007)
Ieda M, Kanazawa H, Kimura K, Hattori F, Ieda Y, Taniguchi M, Lee JK, Matsumura K, Tomita Y, Miyoshi S, Shimoda K, Makino S, Sano M, Kodama I, Ogawa S, Fukuda K. Sema3a maintains normal heart rhythm through sympathetic innervation patterning.Nat Med. (2007)
Sano M., Tokudome S., Shimizu N., Yoshikawa N., Fukuda K. et al. Intramolecular control of protein stability, subnuclear compartmentalization, and coactivator function of PGC-1 ??. J Biol Chem. 282(35):25970-80 (2007)
Endo J, Sano M, Fujita J, Hayashida K, Yuasa S, Aoyama N, Takehara Y, Kato O, Makino S, Ogawa S, Fukuda K.Bone marrow derived cells are involved in the pathogenesis of cardiac hypertrophy in response to pressure overload. Circulation.116(10):1176-84. (2007)

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