作者: Junyan An , Libo Zheng , Shurui Xie , Fengrong Yin , Xiaoxia Huo
DOI: 10.1007/S10620-015-3976-2
关键词:
摘要: Tension homology deleted on chromosome ten (PTEN) is important in liver fibrosis. The purpose of this study was to evaluate the PTEN gene effects and mechanism action hepatic stellate cells (HSCs). rat primary HSCs human LX-2 were transfected by an adenovirus containing cDNA constructs encoding wild-type (Ad-PTEN), mutant G129E (Ad-G129E) RNA interference targeting sequence short hairpin (PTEN shRNA), up-regulate down-regulate expression, respectively. assayed with a fluorescent microscope, real time PCR, Western blot, MTT, flow cytometry Terminal-deoxynucleoitidyl transferase mediated nick end labeling. In addition, CCl4 induced fibrosis model also established check vivo recombinant various levels expression. data have shown that over-expressed led reduced activation viability, caspase-3 activity cell cycle arrest G0/G1 G2/M phases, as well negative regulation PI3K/Akt FAK/ERK signaling pathways vitro. improved function, inhibited proliferation promoted apoptosis both vitro vivo. These therapy using inhibits induces HSCs, which potential treatment option for