Lipopolysaccharide-responsive protein kinase C isotypes in the adult rat aorta.

Abstract

Previous studies have shown that protein kinase C (PKC) activity increases in cardiovascular tissue exposed to lipopolysaccharide (LPS). The objective of these experiments was to identify the PKC isotypes that respond to LPS treatment in the adult rat aorta. We found that PKC alpha, -delta, -epsilon, and -zeta isotypes are present in endothelium-intact aortas. The PKC alpha and -epsilon isotypes show two- to threefold increases in abundance after 3 h treatment with 100 ng/mL LPS, while PKC delta and -zeta levels do not increase. In contrast, mRNA for all of the PKC isotypes increased 3.5 to 12-fold during LPS treatment. Both PKC isotype and mRNA levels gradually diminished during 20 h of continuous LPS exposure. Concurrent treatment of the vessels with LPS plus 50 microM cycloheximide caused PKC alpha, -epsilon, and -zeta, but not -delta, isotypes to rapidly decrease in abundance while blunting the increase in PKC isotype mRNA. The major source for all of the PKC isotypes in the vessel is the vascular smooth muscle cells. These results indicate that LPS treatment induces time-dependent increases in PKC isotype mRNA expression and isotype-specific PKC activation and synthesis in vascular tissue.