title: [The miR-21 attenuates hepatocyte hypoxia/reoxygenation injury via inhibiting PTEN/PI3K/AKT signaling pathway].
abstract: Objective To study the effect of microRNA-21 (miR-21) on hypoxia/reoxygenation (H/R)-treated primary hepatocytes from C57BL/6J mice and analyze its possible molecular mechanism. Methods The H/R model of primary hepatocytes was established and the expression of miR-21 was detected by the quantitative real-time PCR. Western blotting was used to detect protein expression levels of phosphatase and tension homology deleted on chromosome 10 (PTEN), phosphorylated AKT (p-AKT), Bcl-2 and Bax. Flow cytometry was performed to observe the hepatocyte apoptosis. Results The expression of miR-21 in primary hepatocytes decreased after H/R injury. After transfected with exogenous miR-21 mimics, the expression of PTEN decreased, while the expressions of p-AKT and Bcl-2 and the ratio of Bcl-2/Bax increased in hepatocytes; the apoptotic level of hepatocytes was downregulated. The inhibition of AKT phosphorylation could downregulate the expression of Bcl-2 and the ratio of Bcl-2/Bax, and upregulate the level of hepatocyte apoptosis. Conclusion The miR-21 can alleviate the hepatocyte apoptosis by inhibiting the PTEN/PI3K/AKT signaling pathway in the process of H/R.
authors.affiliation: Department of Hepatobiliary Surgery, First Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
authors.forename: Xiuxian
authors.initials: X
authors.lastname: Lu
authors.affiliation: Department of Hepatobiliary Surgery, First Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Sun
authors.affiliation: Department of Hepatobiliary Surgery, First Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
authors.forename: Daofeng
authors.initials: D
authors.lastname: Zheng
authors.affiliation: Department of Hepatobiliary Surgery, First Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
authors.forename: Rui
authors.initials: R
authors.lastname: Liu
authors.affiliation: Department of Hepatobiliary Surgery, First Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
authors.forename: Xufu
authors.initials: X
authors.lastname: Wei
authors.affiliation: Department of Hepatobiliary Surgery, First Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China. *Corresponding author, E-mail: wzjtcy@126.com.
authors.forename: Zhongjun
authors.initials: Z
authors.lastname: Wu
mesh_terms: D000818:Animals; D017209:Apoptosis; D022781:Hepatocytes / Q000166:cytology / Q000201:enzymology* / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000235:genetics / Q000378:metabolism*; D008297:Male; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism*; D051059:PTEN Phosphohydrolase / Q000235:genetics / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D035683:MicroRNAs; D010100:Oxygen; D051059:PTEN Phosphohydrolase; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; C531950:MIRN21 microRNA, mouse