Abstract
Protein kinase C (PKC)-β and other PKC isozymes have been implicated in the loss of endothelial barrier function in diabetic microangiopathy. The effects of a PKC-β-specific inhibitor, LY379196, on hyperpermeability responses to high-glucose, angiotensin II, α-thrombin and endothelin-1 were evaluated using an in vitro model of human pulmonary artery endothelial cell monolayers. LY379196 attenuated the increase in transendothelial albumin flux induced by glucose 40 mM (e.g. 411±160% [high-glucose] vs. 167+37% [high-glucose+LY379196], P<0.001) and angiotensin II 10 μM (e.g. 121±12% vs. 246±35%, P<0.01); endothelin-1 had no significant effect on monolayer permeability. LY379196 had no significant effect on the marked hyperpermeability response to α-thrombin 1 μM. Thus, two major pathways involved in vascular leakage in diabetic microangiopathy are amenable to therapeutic blockade by PKC-β inhibition.
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