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Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
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Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

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Tumor necrosis factor receptor-associated protein 1 regulates hypoxia-induced apoptosis through a

Fei Xiang1, Si-Yuan Ma1, Yan-Ling Lv1

  • 1Institute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038 China.

Burns & Trauma
|May 31, 2019
PubMed
Abstract

Insights

Tumor necrosis factor receptor-associated protein 1 (TRAP1) protects against hypoxia-induced heart cell damage. It regulates apoptosis via a mitochondria-dependent pathway involving cytochrome c oxidase subunit II (COXII) and reactive oxygen species.

Area of Science:

  • Cardiovascular Biology
  • Cellular Stress Response
  • Mitochondrial Function

Background:

  • Tumor necrosis factor receptor-associated protein 1 (TRAP1) exhibits protective effects in hypoxic cardiomyocytes.
  • The exact mechanisms underlying TRAP1's role in hypoxic cardiomyocyte damage remain unclear.

Purpose of the Study:

  • To elucidate the mechanism by which TRAP1 influences hypoxic damage in cardiomyocytes.
  • To investigate the interplay between TRAP1, cytochrome c oxidase subunit II (COXII), and apoptosis in hypoxia.

Main Methods:

  • Utilized overexpression and knockdown techniques to study TRAP1 and COXII in hypoxia-induced cardiomyocytes.
  • Assessed cardiomyocyte apoptosis, mitochondrial cytochrome c release, caspase-3 activity, and reactive oxygen species (ROS) production.

Main Results:

  • TRAP1 overexpression inhibited hypoxia-induced cardiomyocyte apoptosis, while TRAP1 silencing exacerbated it.
  • COXII modulated the effects of TRAP1 on apoptosis; COXII overexpression counteracted TRAP1 silencing effects, and COXII knockdown diminished TRAP1's antiapoptotic function.
  • Changes in apoptosis correlated with mitochondrial cytochrome c release, caspase-3 activation, and ROS levels.

Conclusions:

  • TRAP1 regulates hypoxia-induced cardiomyocyte apoptosis via a mitochondria-dependent pathway.
  • This pathway is mediated by COXII and involves reactive oxygen species as a key component.
Keywords:
ApoptosisCardiomyocytesCytochrome c oxidase subunit IIHypoxiaReactive oxygen speciesTumor necrosis factor receptor-associated protein 1

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