Professional Bio
Dr. Fujiwara received his Ph.D. in Biology from the University of Pennsylvania in 1974. He did his postdoctoral training in Dr. Thomas D. Pollard's laboratory at Harvard Medical School where he worked on the mechanisms of non-muscle cell motility. He was Assistant (1977-1983) and then Associate (1983-1986) Professor in the Department of Anatomy and Cellular Biology, Harvard Medical School where he began analyzing the organization of actin cytoskeleton in vascular endothelial cells in relation to hemodynamic parameters. Dr. Fujiwara was Head of the Department of Structural Analysis in the National Cardiovascular Center Research Institute in Osaka, Japan from 1986 until 2000, when he was recruited to the University of Rochester.
He is past Associate Editor of European Journal of Cell Biology, Biology of the Cell, and Endothelium. He serves on the Editorial Boards of these journals as well as Microvascular Research, Cell Structure and Function, and Bioimages.
Research Bio
Research Overview
Dr. Fujiwara's major research is on mechanosignaling by vascular endothelial cells. Mechanical forces such as fluid flow and stretch trigger unique responses in endothelial cells, indicating that they are capable of sensing mechanical forces. However, the molecular mechanism responsible for this interesting ability of the cells is largely unknown. The recent studies by his research group have indicated that that an endothelial cell adhesion molecule, PECAM-1 (also called CD31) and the actin cytoskeleton are involved in this mechanism. When endothelial cells are exposed to a physiological levels of fluid shear stress, PECAM-1 is rapidly phosphorylated at two tyrosine residues, and this tyrosine phosphorylation appears to be one of the earliest protein modification events one can detect in these cells. Interestingly, PECAM-1 can be also tyrosine phosphorylated by tugging force applied directly to the molecule on the cell surface, suggesting that this molecule is mechanoresponsive. At present, following specific questions are being investigated: (1) what happens to PECAM-1 when mechanical force is applied to it?, (2) how is PECAM-1 tyrosine phosphorylated by mechanical force?, (3) what signaling events are activated by PECAM-1 phosphorylation?, and (4) what role does the actin cytoskeleton play in PECAM-1 signaling? To answer these questions, the laboratory uses techniques of molecular and cell biology, structural analyses, and animal models including PECAM-1 KO mice.
2011
Chang, E.; Heo, K.S.; Woo, C.H.; Lee, H.; Le, N.T.; Fujiwara, K.; Abe, J. "MK2 SUMOylation regulates actin filament remodeling and subsequent migration in endothelial cells by inhibiting MK2 kinase and HSP27 phosphorylation." Blood.. 2011; 117: 2527-2537. |
2010
Shi, F.; Harman, J.; Fujiwara, K.; Sottile, J. "Collagen I matrix turnover is regulated by fibronectin polymerization." Am. J. Physiol. Cell Physiol. 2010; 298: C1265-C1275. |
2010
Nigro, P.; Abe, J.; Woo, C.H.; Satoh, K.; McClain, C.; O'Dell, M.R.; Lee, H.; Lim, J.H.; Li, J.D.; Heo, K.S.; Fujiwara, K.; Berk, B.C. "PKCzeta decreases eNOS protein stability via inhibitory phosphorylation of ERK5". Blood. 2010; 116(11): 1971-1979. |
2008
Chiu, Y-J.; McBeath, E.; Fujiwara, K. "Mechanotransduction in an extracted cell model: Fyn drives stretch and flow-elicited PECAM-1 phosphoryaltion." J Cell Biol. 2008; 182: 753-763. |
2008
Kusano, K.; Thomas, TN.; Fujiwara, K. "Phosphorylation and localization of protein-zero related (PZR) in cultured endothelial cells." Endothelium. 2008; 15: 127-136. |
