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Wei Sheng Wu Xue Bao. 2012 Jul 4;52(7):840-9.

[AMP-activated protein kinase-alpha is involved in the autophagy and apoptosis caused by troglitazone].

[Article in Chinese]

Author information

  • 1State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China. michelle.jinxin@163.com

Abstract

OBJECTIVE:

To reveal the mechanism of AMPK signaling in the autophagy and apoptosis caused by troglitazone (TZ).

METHODS:

To investigate the effect of TZ on alteration of autophagy and apoptosis in HeLa cells, fluorescence microscopy, electron microscopy, western-blotting, siRNA interference, flow cytometry and MTS assay were used.

RESULTS:

TZ attenuated AMP-activated protein kinase-alpha (AMPKalpha) phosphorylation, and stimulates autophagic process in HeLa cells. TZ induced the accumulation of microtubule-associated protein 1 light chain 3-II (LC3-II), and degradation of sequestosome 1 (SQSTM1/p62), two markers of autophagy, occurring prior to the caspase activation. Compound C, an AMPK inhibitor, increased basal and inhibits TZ-stimulated LC3-II content and TZ-depended PARP cleavage. Knockdown of the gene encoding autophagic proteins and AMPK conferred the cells resistance to apoptosis by TZ.

CONCLUSION:

Taken together, these data demonstrate that AMPK is involved in TZ promote autophagy, which precedes and contributes to caspase-dependent apoptosis.

PMID:
23115968
[PubMed - indexed for MEDLINE]
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