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ANGPTL4 attenuates palmitic acid-induced endothelial cell injury by increasing autophagy

Wanlin Zhan1, Wei Tian2, Wenlu Zhang1

  • 1Department of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.

Cellular Signalling
|July 17, 2022
PubMed

Insights

Angiopoietin-like 4 (ANGPTL4) enhances endothelial cell proliferation and protects against injury by regulating autophagy. Lower ANGPTL4 levels are linked to atherosclerosis, suggesting a protective role.

Area of Science:

  • Endocrinology
  • Cardiovascular Biology
  • Cellular Biology

Background:

  • Angiopoietin-like 4 (ANGPTL4) is implicated in various physiological processes, including metabolism and angiogenesis.
  • Previous studies indicated lower plasma ANGPTL4 in coronary atherosclerotic heart disease (CAHD), suggesting a potential role in atherosclerosis.
  • The precise molecular mechanisms of ANGPTL4 in atherosclerosis remain largely unexplored.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which ANGPTL4 influences endothelial cell function and atherosclerosis.
  • To investigate the role of ANGPTL4 in protecting against palmitic acid-induced endothelial cell injury.
  • To explore the relationship between ANGPTL4, autophagy, and atherosclerosis in vitro and in vivo.

Main Methods:

  • Overexpression and knockdown of ANGPTL4 in human umbilical vein endothelial cells (HUVECs).
  • Assessment of endothelial cell proliferation, clone formation, and injury.
  • Investigation of autophagy regulation using autophagy inhibitors (3-MA) and gene knockdown (ATG7).
  • Analysis of ANGPTL4 serum levels and aortic tissue expression in atherosclerosis mouse models.

Main Results:

  • ANGPTL4 overexpression enhanced HUVEC proliferation and clone formation; knockdown had opposite effects.
  • ANGPTL4 expression was upregulated by palmitic acid (PA) and protected against PA-induced endothelial injury.
  • ANGPTL4 promoted endothelial cell proliferation and protected against PA-induced injury by upregulating autophagy.
  • Serum ANGPTL4 levels were decreased in atherosclerosis mice, and its expression correlated with autophagy markers in aortic tissues.

Conclusions:

  • ANGPTL4 promotes endothelial cell proliferation and mitigates palmitic acid-induced endothelial injury via enhanced autophagy.
  • ANGPTL4's protective effects on endothelial cells suggest a potential therapeutic role in preventing atherosclerosis.
  • Downregulation of ANGPTL4 in atherosclerosis indicates its importance in maintaining vascular health.
Keywords:
ANGPTL4AtherosclerosisAutophagyPalmitic acid

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