Premium
Thrombin‐induced glucose transport via Src–p38 MAPK pathway in vascular smooth muscle cells
Author(s) -
Kanda Yasunari,
Watanabe Yasuhiro
Publication year - 2005
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0706293
Subject(s) - thrombin , glut4 , hirudin , glucose transporter , glucose uptake , vascular smooth muscle , mapk/erk pathway , mitogen activated protein kinase , medicine , chemistry , endocrinology , p38 mitogen activated protein kinases , kinase , biology , insulin , biochemistry , platelet , smooth muscle
Thrombin is a mitogen for vascular smooth muscle cells (VSMC) and has been implicated in the development in atherosclerosis. However, little is known about the role of thrombin in glucose transport in VSMC. In this study, we examined the effect of thrombin on glucose uptake in rat A10 VSMC. We found that thrombin induced glucose uptake in a dose‐dependent manner while hirudin, a potent thrombin inhibitor, prevented glucose uptake in the cells. PP2, a selective inhibitor of Src, prevented the thrombin‐induced glucose uptake, but did not affect insulin‐induced uptake. We also examined whether mitogen‐activated protein kinase (MAPK) inhibitors influenced thrombin‐induced glucose uptake. The p38 MAPK inhibitor (SB203580) inhibited thrombin‐induced glucose uptake, but the MEK inhibitor (PD98059) did not. In contrast to thrombin, SB203580 did not affect insulin‐induced glucose uptake. Furthermore, thrombin failed to translocate the insulin‐sensitive glucose transporter GLUT4. These findings suggest that thrombin stimulates glucose transport via Src and subsequent p38 MAPK activation in VSMC.British Journal of Pharmacology (2005) 146 , 60–67. doi: 10.1038/sj.bjp.0706293