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Am J Physiol Heart Circ Physiol (December 9, 2004). doi:10.1152/ajpheart.00382.2004
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Submitted on April 26, 2004
Accepted on December 1, 2004

Strain-induced Vascular Endothelial Cell Proliferation Requires PI3 Kinase Dependent Mammalian Target of Rapamycin-4EBP1 Signal Pathway

Wei Li1 and Bauer E Sumpio1*

1 Department of Surgery, Yale University School of Medicine, New Haven, CT, USA

* To whom correspondence should be addressed. E-mail: bauer.sumpio{at}yale.edu.

The aim of this study was to determine whether the phosphoinositol 3 kinase (PI3K) dependent mammalian target of rapamycin (mTOR)-4EBP1 signal pathway and S6 kinase, the major element of mTOR pathway, play a role in the enhanced vascular endothelial cell (EC)proliferation induced by cyclic strain. Bovine aortic EC were subjected to an average of 10% strain at a rate of 60 cycles/min for up to 24 hours. Cyclic strain-induced EC proliferation was reduced by pre-treatment with rapamycin but not the MEK1 inhibitor, PD98059. The PI3K inhibitors, wortmannin and LY294002, also attenuated strain induced EC proliferation and strain-induced activation of S6 kinase. Rapamycin but not PD98059 prevented strain induced S6 kinase activation and PD 98059, but not rapamycin, prevented strain induced ERK1/2 activation. Cyclic strain also activated 4EBP-1, which could be inhibited by PI3K inhibitors. These data suggest that the PI3K dependent S6 kinas3-mammalian target of rapamycin-4EBP1 signal pathway may be critically involved in the strain induced bovine aortic EC proliferation.




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