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Background  Diabetes mellitus counts as a major risk factor for developing atherosclerosis. The activation of protein kinase C (PKC) is commonly known to take a pivotal part in the pathogenesis of atherosclerosis, though the influence of specific PKC isozymes remains unclear. There is evidence from large clinical trials suggesting excessive neurohumoral stimulation, amongst other pathways leading to PKC activation, as a central mechanism in the pathogenesis of diabetic heart disease. The present study was therefore designed to determine the role of G q -protein signalling via Gα 11  in diabetes for the expression of PKC isozymes in the coronary vessels.    Methods  The role of Gα 11  in diabetes was examined in knockout mice with global deletion of Gα 11  compared to wildtype controls. An experimental type 1-diabetes was induced in both groups by injection of streptozotocin. Expression and localization of the PKC isozymes α, βII, δ, ε, and ζ was examined by quantitative immunohistochemistry.    Results  8 weeks after induction of diabetes a diminished expression of PKC  ε  was observed in wildtype animals. This alteration was not seen in Gα 11  knockout animals, however, these mice showed a diminished expression of PKCζ. Direct comparison of wildtype and knockout control animals revealed a diminished expression of PKC δ and ε in Gα 11  knockout animals.    Conclusion  The present study shows that expression of the nPKCs δ and  ε  in coronary vessels is under control of the g-protein Gα 11 . The reduced expression of PKC ζ that we observed in coronary arteries from Gα 11 -knockout mice compared to wildtype controls upon induction of diabetes could reduce apoptosis and promote plaque stability. These findings suggest a mechanism that may in part underlie the therapeutic benefit of RAS inhibition on cardiovascular endpoints in diabetic patients.

Differential expression of protein kinase C isoforms in coronary arteries of diabetic mice lacking the G-protein Gα11