Ablation of TMEM126B protects against oxygen-glucose deprivation/reoxygenation-induced injuries of PC12  cells via maintaining mitochondrial anti-apoptotic functions.

Ablation of TMEM126B protects against oxygen-glucose deprivation/reoxygenation-induced injuries of PC12 cells via maintaining mitochondrial anti-apoptotic functions. Arch Biochem Biophys. 2020 Oct 16;:108634 Authors: Wei L, Fan Y, Wei L, He X, Yang J, Zheng X Abstract Ischemia reperfusion (I/R) injury is a key contributing factor to the pathogenic mechanism involved in cerebral infarction. Transmembrane protein 126b (TMEM126B), a mitochondrial complex I assembly factor, has been reported to have an intimate association with disease progression, but is little known in ischemia stroke. The present study was designed to explore the effects of TEME126B on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced neuronal PC12 cells. The mRNA level of TMEM126B was determined using qRT-PCR. The levels of ROS, MDA, and SOD, as well as inflammatory cytokines, were measured using corresponding commercial kits. Cell apoptosis rate was assayed by flow cytometry analysis, and the apoptosis-related proteins were measured using western blotting. ATP production measured by colorimetric reaction and mitochondrial membrane potential measured by JC-1 staining were conducted to determine mitochondrial dysfunction. The results showed that TMEM126B was upregulated upon I/R injury in vitro and in clinical, and was positively corrected with the degree of oxidative stress. TMEM126B knockdown significantly reduced oxidative stress and inflammation in OGD/...
Source: Archives of Biochemistry and Biophysics - Category: Biochemistry Authors: Tags: Arch Biochem Biophys Source Type: research