p66Shc Mediates Mitochondrial Dysfunction Dependent on PKC Activation in Airway Epithelial Cells Induced by Cigarette Smoke

Oxidative Medicine and Cellular Longevity
Ming ZhangYali Li

Abstract

Airway epithelial mitochondrial injury plays a critical role in the pathogenesis of chronic obstructive pulmonary disease (COPD). The p66Shc adaptor protein is a newly recognized mediator of mitochondrial dysfunction. However, little is known about the effect of p66Shc on airway epithelial damage in the development of COPD. The aim of the present study is to investigate the roles of p66Shc and its upstream regulators in the mitochondrial injury of airway epithelial cells (Beas-2b) induced by cigarette smoke extract (CSE). Our present study revealed that CSE increased p66Shc expression and its mitochondrial translocation in concentration and time-dependent manners in airway epithelial cells. And p66Shc siRNA significantly attenuated mitochondrial dysfunction and cell injury when airway epithelial cells were stimulated with 7.5% CSE. The total and phosphorylated expression of PKCβ and PKCδ was significantly increased associated with mitochondrial dysfunction and cell injury when airway epithelial cells were exposed to 7.5% CSE. The pretreatments with pharmacological inhibitors of PKCβ and PKCδ could notably suppress p66Shc phosphorylation and its mitochondrial translocation and protect the mitochondria and cells against oxidative...Continue Reading

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Citations

Jun 6, 2019·Basic Research in Cardiology·Kerstin BoenglerRainer Schulz
Oct 3, 2020·Oxidative Medicine and Cellular Longevity·Ming ZhangJie Zhang
Nov 12, 2020·American Journal of Physiology. Lung Cellular and Molecular Physiology·Jennifer M K NguyenVenkataramana K Sidhaye
Feb 20, 2021·Journal of Experimental Pharmacology·Gundula Schulze-Tanzil
Dec 7, 2019·Biochemical and Biophysical Research Communications·Shuyu PiaoCuk-Seong Kim

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Methods Mentioned

BETA
PCR
ELISA
protein assay
electrophoresis
confocal
flow cytometry

Software Mentioned

Pro Plus
Image
Bandscan
SPSS

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