p62 Sequestosome 1/Light Chain 3b Complex Confers Cytoprotection on Lung Epithelial Cells after Hyperoxia

• DOI: 10.1165/rcmb.2012-0017oc
• Publication Date: 2013-01-19T01:16:57Z
• Authors: Xiaoliang Liang; Shu-Quan Wei; Seon-Jin Lee; James K. Fung; Meng Zhang; Akihiko Tanaka; Augustine M. K. Choi; Yang Jin
• Keywords: Hyperoxia; Cytoprotection; Sequestosome 1

Lung epithelial cell death is a prominent feature of hyperoxic lung injury, and has been considered very important underlying mechanism acute injury (ALI) respiratory distress syndrome (ARDS). Here we report on novel involved in cytoprotection homeostasis after oxidative stress. p62 (sequestosome 1; SQSTM1) ubiquitously expressed cellular protein. It interacts with ubiquitinated proteins autophagic marker light chain 3b (LC3b), thus mediating the degradation selective targets. In this study, explored role mitochondria-mediated hyperoxia. alveolar cells demonstrate abundant expression, concentrations are up-regulated by stress at both protein mRNA levels. The p62/LC3b complex Fas truncated BID (tBID) physically. These interactions abruptly diminish deletion robustly increases tBID cleaved caspase-3, implying an antiapoptotic effect. This effect further confirmed measuring caspase activities, poly ADP ribose polymerase, viability. PBI domain or ubiquitin-associated lead to elevated tBID, significantly more Moreover, traffics opposite direction LC3b hyperoxia, leading dissociation p62/Cav-1/LC3b/BID complex. Subsequently, LC3b-mediated lysosomal eliminated. Taken together, our data suggest that regulates