BRCC36 promotes intestinal mucosal barrier injury caused by BMP2 after ischemia reperfusion via inhibiting PPARγ signaling

Biosci Biotechnol Biochem. 2022 Feb 24;86(3):331-339. doi: 10.1093/bbb/zbab210.

Abstract

As one of the most common pathological changes in trauma and surgery practice, intestinal ischemia-reperfusion (I/R) injury is regarded as a major precipitating factor in the occurrence and development of fatal diseases. BRCA1-BRCA2-containing complex subunit 36 (BRCC36), a deubiquitinase, has been proved important in a variety of pathophysiological processes such as DNA repair, cell cycle regulation, tumorigenesis, and inflammatory response. However, the effect of BRCC36 on intestinal mucosal barrier injury after I/R has not been fully elucidated. Our research found that BRCC36 aggravated intestinal mucosal barrier injury caused by bone morphogenetic protein 2 after I/R by downregulating peroxisome proliferator-activated receptor-γ (PPARγ) signaling. These results suggested that BRCC36/PPARγ axis might serve as a potential therapeutic target for preventing intestinal mucosal barrier injury after I/R.

Keywords: BRCC36; Ischemia reperfusion; PPARγ; intestinal barrier injury.

MeSH terms

  • PPAR gamma*

Substances

  • PPAR gamma