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Updated: Mar 15, 2026

On-Chip Endothelial Inflammatory Phenotyping
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APOC3 induces endothelial dysfunction through TNF-α and JAM-1

Yun Tao1, Yisong Xiong2, Huimin Wang1

  • 1Center of Laboratory Medicine, Affiliated Hospital, Nantong University, 20 Xi Si Road, Nantong, 226001, People's Republic of China.

Lipids in Health and Disease
|September 14, 2016
PubMed

Insights

Apolipoprotein C3 (APOC3) promotes cardiovascular disease (CVD) by increasing inflammation and endothelial cell (EC) dysfunction. Targeting APOC3-induced inflammation may offer a novel therapeutic strategy for CVD.

Area of Science:

  • Lipid metabolism and cardiovascular research
  • Endothelial cell biology
  • Inflammation and atherosclerosis

Background:

  • Cardiovascular disease (CVD) fatality rates are rising, with elevated triglycerides as a risk factor.
  • Endothelial cell (EC) dysfunction is a key contributor to CVD.
  • Apolipoprotein C3 (APOC3) is linked to hyperlipidemia and CVD risk, but its direct effects on ECs were unclear.

Purpose of the Study:

  • To determine the direct effects of APOC3 on ECs.
  • To investigate APOC3's role in EC inflammation, chemotaxis, and exudation.

Main Methods:

  • Utilized ELISA, qRT-PCR, immunofluorescence, flow cytometry, and transwell assays on human umbilical vein endothelial cells (HUVECs).
  • Employed siRNA to silence TNF-α and JAM-1 to analyze APOC3's influence on EC inflammatory processes.

Main Results:

  • APOC3 correlated with EC inflammation, marked by increased TNF-α expression.
  • APOC3 disrupted endothelial tight junctions (TJs) via elevated JAM-1, promoting leukocyte exudation and EC chemotaxis.
  • APOC3 increased THP-1 cell adhesion to HUVECs.

Conclusions:

  • Elucidated the mechanism of APOC3-induced EC inflammation, chemotaxis, and exudation.
  • Suggests targeting APOC3-mediated inflammatory pathways as a potential new therapeutic approach for CVD.
Abstract

Keywords:
APOC3Cardiovascular diseaseEndothelial dysfunctionInflammation

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