Depletion of SENP1-mediated PPARγ SUMOylation exaggerates intermittent hypoxia-induced cognitive decline by aggravating microglia-mediated neuroinflammation.

ABSTRACT: Intermittent hypoxia (IH)-associated cognition decline is related to the neuroinflammation of microglia. SUMOylation is a post-translational modification related to multiple human diseases, which can be reversed by SENP1. Studies showed that SENP1 and PPARγ play essential roles in restricting inflammation by blocking NF-κB activation. However, the mechanism remains unclear. Herein, we investigated the precise mechanism underlying SENP1 and PPARγ in cognitive decline after IH insult. Biochemical analysis results revealed that IH triggered the inflammatory response and neuronal apoptosis, increased the SUMOylation of PPARγ, and decreased the level of PPARγ compared to that in the normoxia group. After SENP1 downregulation, the inflammatory response, neuronal apoptosis and the SUMOylation of

SUBMITTER: Wang H 

PROVIDER: S-EPMC8221356 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature