Role for PKC-epsilon in neuronal death induced by oxidative stress

Biochemical and Biophysical Research Communications
Yi-Sook JungChang-Hyun Moon

Abstract

We investigated which isoforms of PKCs can be modulated and what their roles are during l-buthionine-S,R-sulfoximine (BSO)-induced neuronal death. We observed the isoform specific translocation of PKC-epsilon from the soluble fraction to the particulate in cortical neurons treated with 10 mM BSO. The translocation of PKC-epsilon by BSO was blocked by antioxidant trolox, suggesting the PKC-epsilon as a downstream of reactive oxygen species (ROS) elevated by BSO. Trolox inhibited the ROS elevation and the neuronal death in BSO-treated cortical cells. The BSO-induced neuronal death was remarkably inhibited by both the pharmacological inhibition of PKC-epsilon with epsilonV1-2 and the functional blockade for PKC-epsilon through overexpression of PKC-epsilon V1 region, suggesting the detrimental role of PKC-epsilon. These results suggest that PKC-epsilon is the major PKC isoform involved in the pathways triggered by ROS, leading to neuronal death in BSO-treated cortical neurons.

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Citations

Jan 6, 2006·Archives of Pharmacal Research·Mi-Young KimYi-Sook Jung
Aug 21, 2009·American Journal of Physiology. Renal Physiology·Vijayalakshmi ThamilselvanSivagnanam Thamilselvan
Aug 17, 2005·Cancer Research·Hana OkhrimenkoChaya Brodie
Sep 18, 2010·Chemosphere·Hyun-Gyo Lee, Jae-Ho Yang
Sep 27, 2016·Oxidative Medicine and Cellular Longevity·Bo Kyung Lee, Yi-Sook Jung
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Mar 31, 2005·The Journal of Pharmacology and Experimental Therapeutics·Brian E ReeseJong Yun
Nov 12, 2017·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Daniela Di MarcantonioStephen M Sykes
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Jun 21, 2011·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·Sukanya PhalitakulHideyuki Yamawaki

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