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Activation of pannexin-1 mediates triglyceride-induced macrophage cell death

Byung Chul Jung1, Sung Hoon Kim2, Jaewon Lim3

  • 1Department of Nutritional Sciences and Toxicology, University of California, Berkeley, CA 94720, United States; Department of Biomedical Laboratory Science, College of Health Sciences, Yonsei University, Wonju 26493, Korea.

BMB Reports
|October 14, 2020
PubMed

Insights

Triglyceride accumulation in macrophages causes cell death, a risk factor for atherosclerosis. This study reveals that pannexin-1 activation, leading to potassium efflux, drives this cell death.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pathology

Background:

  • Triglyceride accumulation in macrophages is a risk factor in atherosclerosis pathogenesis.
  • Previous work identified caspase-1 and -2 as triggers for TG-induced macrophage death.

Purpose of the Study:

  • To investigate the mechanism of triglyceride-induced macrophage cell death.
  • To elucidate the role of potassium efflux and pannexin-1 in this process.

Main Methods:

  • Utilized THP-1 macrophages treated with triglycerides.
  • Measured potassium efflux, ATP concentration, and caspase activation.
  • Assessed the effects of pannexin-1 inhibition using probenecid.

Main Results:

  • Triglyceride treatment increased potassium efflux and pannexin-1 activation in macrophages.
  • Inhibiting potassium efflux or pannexin-1 blocked TG-induced cell death and caspase activation.
  • Reducing ATP concentration restored cell viability and caspase activity.

Conclusions:

  • Triglyceride-induced macrophage cell death is mediated by pannexin-1 activation.
  • This activation leads to increased extracellular ATP and subsequent potassium efflux.
  • The findings provide a novel mechanism linking lipid accumulation to inflammatory cell death in atherosclerosis.

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