1978 - Ph.D., Pharmacology, University of Tokyo School of Medicine, Tokyo, Japan
1969 - M.S., Biophysics, Waseda University School of Science and Engineering, Tokyo, Japan
1967 - B.S., Applied Physics, Waseda University School of Science and Engineering, Tokyo, Japan
My research interests involve physiology, molecular biology and pathology of the signal transduction mechanism in vascular smooth muscle contraction and relaxation to elucidate human vascular diseases. Smooth muscle contraction and relaxation is primarily regulated by reversible phosphorylation of myosin light chain (MLC), the extent of which is determined by the balance between MLC kinase (MLCK) and MLC phosphatase (MLCP) activity. To the classical hypothesis of the Ca2+-dependent MLCK, we have recently added a new idea of rapid Ca2+-dependent MLCP regulation in peripheral resistance arteries, which have a key role in the fine-tuning of blood pressure during movement. There are, however, some other circulation systems in our body including cerebral, pulmonary and cardiac circulations. Interestingly, a set of key players in each system may differ from others, depending upon their physiological demands. Those are our current and next targets.
Our research is to elucidate mechanism of blood circulation system in molecular levels. From these basic researches, we believe to gain a better understanding of circulation system and to suggest new strategies for therapy of human disease.
T. Kitazawa and K. Kitazawa. Size-dependent heterogeneity of contractile Ca2+- sensitization in rat arterial smooth muscle. J. Physiol. 590, 5401-5423, 2012. PMID: 22930267.
Y.H. Huh, Q. Zhou, J.K. Liao, and T. Kitazawa. ROCK inhibition prevents fetal serum- induced alteration in structure and function of organ-cultured mesenteric artery. J. Muscle Res. Cell Motil. 32, 65-76, 2011. PMID: 21643972.
A. Hishiya, T. Kitazawa, and S. Takayama. BAG3 and Hsc70 interact with actin capping protein CapZ to maintain myofibrillar integrity under mechanical stress. Circ. Res. 107, 1220-1231, 2010. PMID: 20884878.
T. Kitazawa. G Protein-Mediated Ca2+-Sensitization of CPI-17 Phosphorylation in Arterial Smooth Muscle. Biochem. Biophys. Res. Commun. 401, 75-78, 2010. PMID: 20833141
T. Kitazawa, S. Semba, Y-H. Huh, K. Kitazawa, and M. Eto. Nitric Oxide-Induced Biphasic Mechanism of Vascular Relaxation via Dephosphorylation of CPI-17 and MYPT1. J. Physiol. 587, 3587–3603, 2009. Cited in the Editor’s Perspectives. PMID: 19470783.
M. Eto, T. Kitazawa, F. Matsuzawa, S. Aikawa, J. A. Kirkbride, N. Isozumi, Y. Nishimura, D. L. Brautigan, and S. Ohki. Phosphorylation-induced conformational switching of CPI-17 produces a potent myosin phosphatase inhibitor. Structure 15, 1591–1602, 2007. PMID: 18073109.
G. Dimopoulos, S. Semba, K. Kitazawa, M. Eto and T. Kitazawa. Ca2+-dependent rapid Ca2+ sensitization of contraction in arterial smooth muscle. Circ. Res. 100, 121-129, 2007. Cited in the Editorials. PMID: 17158339.
X. Ai, T. Kitazawa, A-T. Do, M. Kusche-Gullberg, P. A. Labosky and C. P. Emerson, Jr. SULF1 and SULF2 regulate heparan sulfate-mediated GDNF signaling for esophageal innervation. Development 134, 3327-3338, 2007. PMID: 17720696.
T. Woodsome, A. Polzin, K. Kitazawa, M. Eto and T. Kitazawa. Agonist- and depolarization-induced signals for myosin light chain phosphorylation and force generation of cultured vascular smooth muscle cells. J. Cell Sci. 119, 1769-1780, 2006. PMID: 16608882.
M. Eto, T. Kitazawa and D. L. Brautigan. Phosphoprotein inhibitor CPI-17 specificity depends on allosteric regulation of protein phosphatase-1 by regulatory subunits. Proc. Natl. Acad. Sci. USA. 101, 8888-8893, 2004. PMID: 15184667.
T. Kitazawa, A. Polzin and M. Eto. CPI-17-deficient smooth muscle of chicken. J. Physiol. 557, 515-528, 2004. PMID: 15090608.
T. Kitazawa, M. Eto, T. P. Woodsome and M. Khalequzzaman. Phosphorylation of the myosin phosphatase targeting subunit and CPI-17 during Ca2+ sensitization in rabbit smooth muscle. J. Physiol. 546, 879-889, 2003. PMID: 12563012.
M. Eto, T. Kitazawa, M. Yazawa, H. Mukai, Y. Ono, and D. L. Brautigan. Histamine- induced vasoconstriction involves phosphorylation of a specific inhibitor protein for myosin phosphatase by protein kinase C a and d isoforms. J. Biol. Chem. 276, 29072-29079, 2001. PMID: 11397799.
T.P. Woodsome, M. Eto, A. Everett, D. L. Brautigan, and T. Kitazawa. Expression of CPI- 17 and myosin phosphatase correlates with Ca2+ sensitivity of protein kinase C- induced contraction in rabbit smooth muscle. J. Physiol. 535, 553-564, 2001. PMID: 11533144.
T. Kitazawa, M. Eto, T. P. Woodsome and D. L. Brautigan. Agonists trigger G protein- mediated activation of the CPI-17 inhibitor phosphoprotein of myosin light chain phosphatase to enhance vascular smooth muscle contractility. J. Biol. Chem. 275, 9897-9900, 2000. PMID: 10744661.