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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

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

Xin Jin1, Dongdong Yuan, Xiuling Chen

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

Wei Sheng Wu Xue Bao = Acta Microbiologica Sinica
|November 3, 2012
PubMed
Abstract

Insights

Troglitazone (TZ) activates autophagy via AMP-activated protein kinase (AMPK) signaling, preceding apoptosis. Inhibiting AMPK blocks TZ-induced autophagy and cell death, revealing AMPK

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Troglitazone (TZ) is known to induce cell death.
  • The precise mechanisms underlying TZ-induced apoptosis and autophagy remain incompletely understood.
  • AMP-activated protein kinase (AMPK) signaling pathways are implicated in cellular stress responses.

Purpose of the Study:

  • To elucidate the role of AMPK signaling in troglitazone-induced autophagy and apoptosis.
  • To investigate the temporal relationship between autophagy and apoptosis.
  • To determine if AMPK activation is a prerequisite for TZ-induced cell death.

Main Methods:

  • HeLa cells were treated with troglitazone (TZ).
  • Autophagy was assessed using markers like LC3-II and SQSTM1/p62 via western blotting.
  • Apoptosis was evaluated through caspase activation and PARP cleavage.
  • AMPK activity was modulated using siRNA interference and the inhibitor Compound C.
  • Cell viability was measured using MTS assay.

Main Results:

  • TZ treatment reduced AMPK phosphorylation and stimulated autophagy in HeLa cells.
  • TZ induced accumulation of LC3-II and degradation of SQSTM1/p62, preceding caspase activation.
  • AMPK inhibition by Compound C blocked TZ-stimulated autophagy and PARP cleavage.
  • Knockdown of autophagy-related genes or AMPK conferred resistance to TZ-induced apoptosis.

Conclusions:

  • AMPK signaling is crucial for mediating troglitazone-induced autophagy.
  • TZ-induced autophagy precedes and contributes to caspase-dependent apoptosis.
  • Targeting the AMPK-autophagy pathway may offer therapeutic strategies for TZ-related effects.

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