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Am J Physiol Cell Physiol 279: C587-C595, 2000;
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Vol. 279, Issue 3, C587-C595, September 2000

Acute glucose-induced downregulation of PKC-beta II accelerates cultured VSMC proliferation

Mayumi Yamamoto1, Mildred Acevedo-Duncan3, Charles E. Chalfant1, Niketa A. Patel1, James E. Watson3, and Denise R. Cooper1,2,3

1 Department of Biochemistry and Molecular Biology and 2 Department of Internal Medicine, University of South Florida, College of Medicine, and 3 Research Service, J. A. Haley Veterans Hospital, Tampa, Florida 33612

Accelerated vascular smooth muscle cell (VSMC) proliferation contributes to the formation of atherosclerotic lesions. To investigate protein kinase C (PKC)-beta II functions with regard to glucose-induced VSMC proliferation, human VSMC from aorta (AoSMC), a clonal VSMC line of rat aorta (A10), and A10 cells overexpressing PKC-beta I (beta I-A10) and PKC-beta II (beta II-A10) were studied with the use of three techniques to evaluate glucose effects on aspects affecting proliferation. High glucose (25 mM) increased DNA synthesis and accelerated cell proliferation compared with normal glucose (5.5 mM) in AoSMC and A10 cells, but not in beta I-A10 and beta II-A10 cells. The PKC-beta II specific inhibitor CGP-53353 inhibited glucose-induced cell proliferation and DNA synthesis in AoSMC and A10 cells. In flow cytometry analysis, high glucose increased the percentage of A10 cells at 12 h after cell cycle initiation but did not increase the percentage of beta I-A10 or beta II-A10 cells entering S phase. PKC-beta II protein levels decreased before the peak of DNA synthesis, and high glucose further decreased PKC-beta II mRNA and protein levels in AoSMC and A10 cells. These results suggest that high glucose downregulates endogenous PKC-beta II, which then alters the normal inhibitory role of PKC-beta II in cell cycle progression, resulting in the stimulation of VSMC proliferation through acceleration of the cell cycle.

atherosclerosis; cell cycle; diabetes mellitus; protein kinase C inhibitor; thymidine


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