HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 295/5/H2135    most recent 00704.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Descorbeth, M. Articles by Anand-Srivastava, M. B. Search for Related Content PubMed PubMed Citation Articles by Descorbeth, M. Articles by Anand-Srivastava, M. B.

High glucose increases the expression of G_q/11 and PLC-β proteins and associated signaling in vascular smooth muscle cells

Department of Physiology, Faculty of Medicine, University of Montreal, Montreal, Quebec, Canada

Submitted 9 July 2008 ; accepted in final form 18 September 2008

The levels and activity of protein kinase C and diacylglycerol were shown to be upregulated in diabetes/hyperglycemia; however, studies on the expression of upstream signaling molecules of phosphatidylinositol turnover were lacking. The present study was therefore undertaken to examine whether hyperglycemia/diabetes could also modulate the expression of G_q and phospholipase C-β (PLC-β) proteins and associated phosphatidylinositol turnover signaling in aortic vascular smooth muscle cells (VSMCs) and A10 VSMCs exposed to high glucose. Aortic VSMCs from streptozotocin-diabetic rats exhibited an increased expression of G_q and PLC-β₁ proteins (60% and 30%, respectively) compared with control cells as determined by Western blot analysis. The pretreatment of A10 VSMCs with high glucose (26 mM) for 3 days also augmented the levels of G_q, G11, PLC-β₁ and -β₂ proteins by about 50, 35, 30, and 30%, respectively, compared with control cells that were restored to control levels by endothelin-1 (ET-1), ET types A and B (ET_A and ET_B) receptors, and angiotensin II type 1 (AT₁) receptor antagonists. In addition, ET-1-stimulated inositol triphosphate formation was also significantly higher in VSMCs exposed to high glucose, whereas the basal levels of inositol triphosphate were not different between the two groups. Furthermore, the treatment of A10 VSMCs with angiotensin II and ET-1 also significantly increased the levels of G_q/11 and PLC-β proteins that were restored toward control levels by ET_A/ET_B and AT₁ receptor antagonists. These results suggest that high glucose augments the expression of G_q/11, PLC-β, and mediated signaling in VSMCs, which may be attributed to AT₁, ET_A, and ET_B receptors.

G_q protein; phospholipase C-β; phosphatidylinositol turnover