PKC epsilon facilitates recovery of exocytosis after an exhausting stimulation
Date of Issue2009
School of Chemical and Biomedical Engineering
It has been well documented that protein kinase Cs (PKCs) play multifaceted roles in regulating exocytosis of neurotransmitters and hormones. But the isoform-specific PKC effects are still poorly elucidated mainly because of the large variety of PKC isoforms and the dubious specificity of the commonly used pharmacological agents. In the present study, based on overexpression of wild-type or dominant negative PKCε, we demonstrate in neuroendocrine PC12 cells that PKCε, but not PKCα, facilitates recovery of exocytosis after an exhausting stimulation. Specifically, PKCε mediates fast recovery of the extent of exocytosis in a phosphatidylinositol biphosphate-dependent manner, likely through enhancing the rate of vesicle delivery and reorganization of cortical actin network. In addition, PKCε promotes fast recovery of vesicle release kinetics that is slowed after a strong stimulation. These experimental results may suggest a PKC-dependent mechanism relevant to the short-term plasticity of exocytosis in both neurons and neuroendocrine cells.
Pflügers archiv European journal of physiology
© 2009 Springer-Verlag. This is the author created version of a work that has been peer reviewed and accepted for publication by Pflügers Archiv European Journal of Physiology, Springer-Verlag. It incorporates referee’s comments but changes resulting from the publishing process, such as copyediting, structural formatting, may not be reflected in this document. The published version is available at: [DOI: http://dx.doi.org/10.1007/s00424-009-0697-4].