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Complement C3 Reduces Apoptosis via Interaction with the Intrinsic Apoptotic Pathway

Zhou Fang1, Haekyung Lee1, Junying Liu1

  • 1Departments of Anesthesiology, SUNY Downstate Health Science University, 450 Clarkson Avenue, Brooklyn, NY 11203, USA.

Cells
|September 28, 2023
PubMed

Insights

Complement C3 significantly reduces heart cell apoptosis after ischemia/reperfusion injury. This protein interacts with the intrinsic apoptosis pathway, offering a potential therapeutic target for heart attack recovery.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Cellular Apoptosis

Background:

  • Myocardial ischemia/reperfusion (I/R) injury triggers inflammation involving complement factors.
  • Previous studies indicated reduced necrosis in complement C3-deficient mice post-I/R.
  • The role of C3 in myocardial apoptosis remained to be elucidated.

Purpose of the Study:

  • To investigate the effect of complement C3 on myocardial apoptosis following I/R injury.
  • To determine if C3 regulates apoptosis in human cardiomyocytes.
  • To explore the molecular mechanisms underlying C3's action on apoptosis.

Main Methods:

  • Utilized a mouse model of heart I/R.
  • Employed comparative proteomics to identify proteins within the myocardial C3 complex.
  • Conducted cell culture experiments with human cardiomyocytes and a cell-free apoptosis system.

Main Results:

  • Cytochrome c was identified within the myocardial C3 complex in wild-type mice post-I/R.
  • Exogenous human C3 reduced apoptosis in human cardiomyocytes lacking endogenous C3.
  • Human C3 inhibited the intrinsic apoptosis pathway in a cell-free system and bound pro-caspase 3.

Conclusions:

  • Complement C3 plays a protective role by reducing myocardial apoptosis after I/R injury.
  • C3 directly interacts with the intrinsic apoptosis pathway, involving pro-caspase 3.
  • These findings highlight C3 as a potential therapeutic target for mitigating I/R-induced cardiac damage.

Keywords:
apoptosiscomplement C3cytochrome cischemia/reperfusion injury (IRI)pro-caspase 3

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