Changman Zhou

Changman Zhou

Peking University Health Science Center, China

Title: TMEM166 knockdown attenuates ischemic-induced neuronal autophagy via mTOR pathway in mice


Changman Zhou, Professor in Department of Anatomy and Histology at Peking University Health Science Center, China. Currently Vice-President and General Secretary of Chinese Society of Anatomical Sciences (CSAS). Changman Zhou current research focus is preclinical translational research related to the neuronal regeneration and neurobiology of diseases such as stroke. He published more than 120 international papers and many book chapters. He is currently on the Editorial Boards of Clinical Anatomical, Anatomical Record, Anatomy & Cell Biology and Vice Editor-in- Chief of Acta Anatomica Sinica .


Transmembrane protein 166 (TMEM166), also known as FAM176A, is located on chromosome 2p12. Recent studies have shown that over-expression of TMEM166 markedly inhibits the proliferation of tumor cells and induces both cell autophagy and apoptosis. It was also found had a significant increase after MCAO. However, the role of TMEM166 involved in this process is still unknown. To determine the role of TMEM166 following MCAO injury, 156 male C57 mice were randomly divided into 4 groups: Sham, MCAO (wild type), MCAO (TMEM166 knockout), MCAO+ Rapamycin (mTOR inhibitor, ip, 0.5 ng in 0.5 ul 0.1% DMSO , 20 min before MCAO), MCAO+ shTSC2 (mTOR activator,i.c.v, 5ul immediately after MCAO). TTC, neurological scores, mortality rate, brain water content, TUNEL staining, western blot and immunohistochemistry (Beclin-1, LC-,mTOR,p-mTOR,p70s6k,p-p70s6k) were conducted 24 h following MCAO. The results show that TMEM166 knockdown inhibits autophagy and improves brain injury following MCAO in mice. Compared with untreatd c57 mince, rapamycin treated mice shows downregulation of mTOR and upregulation of TMEM166 by western blot and immunohistochemistry. Treatment with TSC2 shRNA increases the expression of mTOR and decreases the expression of TMEM166.

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