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缺氧诱导因子-1α调节自噬以激活肝星状细胞。

Hypoxia-inducible factor-1alpha regulates autophagy to activate hepatic stellate cells.

作者信息

Deng Jing, Huang Qin, Wang Yueqin, Shen Pei, Guan Fei, Li Jianrong, Huang Hanju, Shi Chunwei

机构信息

Department of Pathogen Biology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China.

Department of Medical Rehabilitation, Union Hospital, Huazhong University of Science and Technology, Wuhan 430030, PR China.

出版信息

Biochem Biophys Res Commun. 2014 Nov 14;454(2):328-34. doi: 10.1016/j.bbrc.2014.10.076. Epub 2014 Oct 22.

DOI:10.1016/j.bbrc.2014.10.076
PMID:25450397
Abstract

The role of autophagy in Hif-1α modulated activation of hepatic stellate cells was illustrated in current work. Autophagy markers were determined in livers of Schistosoma japonicum infected mice and hypoxia or LPS treated human hepatic stellate cell, LX-2 cells. The action of Hif-1 to autophagy was defined as increase of autophagy markers was significantly suppressed in Hif-1α siRNA transfected cells upon hypoxia or LPS stimulation. The function of autophagy in activation of LX-2 cells was assessed as increase of activation markers was blocked using autophagy inhibitors under hypoxia and LPS stimulation. Conclusively, Hif-1α regulates activation of hepatic stellate cell by modulating autophagy.

摘要

本研究阐述了自噬在Hif-1α调节肝星状细胞激活中的作用。在日本血吸虫感染小鼠的肝脏以及缺氧或脂多糖处理的人肝星状细胞LX-2中测定自噬标志物。Hif-1对自噬的作用表现为,在缺氧或脂多糖刺激下,Hif-1α siRNA转染细胞中自噬标志物的增加受到显著抑制。在缺氧和脂多糖刺激下,使用自噬抑制剂阻断激活标志物的增加,以此评估自噬在LX-2细胞激活中的作用。总之,Hif-1α通过调节自噬来调控肝星状细胞的激活。

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