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Updated: Jan 27, 2026

Isolation and Primary Culture of Mouse Aortic Endothelial Cells
08:20

Isolation and Primary Culture of Mouse Aortic Endothelial Cells

Published on: December 19, 2016

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CTRP3 Alleviates Ox-LDL-Induced Inflammatory Response and Endothelial Dysfunction in Mouse Aortic Endothelial Cells

Lei Chen1, Lijun Qin2, Xin Liu3

  • 1Department of Critical Care Medicine, Gansu Provincial Hospital of TCM, No. 418, Guazhou Road, Qilihe District, Lanzhou City, 730050, Gansu, People's Republic of China. chenleiccm@163.com.

Inflammation
|March 20, 2019
PubMed

Insights

C1q/tumor necrosis factor-related protein-3 (CTRP3) protects against atherosclerosis by reducing inflammation and endothelial dysfunction. This adipokine activates the PI3K/Akt/eNOS pathway, offering a potential therapeutic strategy.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Adipokine Research

Background:

  • Atherosclerosis involves plaque rupture and thrombosis, leading to cardiovascular events.
  • The role of C1q/tumor necrosis factor-related protein-3 (CTRP3) in atherosclerosis is not fully understood.
  • Oxidized low-density lipoprotein (ox-LDL) is a key factor in endothelial dysfunction and inflammation.

Purpose of the Study:

  • To investigate the protective effects of CTRP3 against ox-LDL-induced inflammation and endothelial dysfunction.
  • To elucidate the underlying molecular mechanisms of CTRP3 action in mouse aortic endothelial cells.
  • To assess CTRP3's potential as a therapeutic target for atherosclerosis.

Main Methods:

  • CTRP3 expression was analyzed in ApoE-/- mice and normal mice.
  • Mouse aortic endothelial cells were treated with ox-LDL and transfected with pcDNA-CTRP3 or siCTRP3.
  • Inflammatory markers (CRP, TNF-α, IL-6, CD40, CD40L), cell viability, apoptosis, adhesion molecules (ICAM-1, VCAM-1), and signaling pathways (PI3K/Akt/eNOS) were assessed.
  • Pathway inhibitors (LY294002, L-NAME) were used to confirm the mechanism.

Main Results:

  • CTRP3 expression was reduced in ApoE-/- mice.
  • Overexpression of CTRP3 downregulated inflammatory cytokines and adhesion molecules.
  • CTRP3 enhanced cell activity, reduced apoptosis, and restored the balance of vasoactive factors (ET-1/NO).
  • CTRP3 activated the PI3K/Akt/eNOS pathway, which was essential for its protective effects.

Conclusions:

  • CTRP3 ameliorates ox-LDL-induced inflammation and endothelial dysfunction in mouse aortic endothelial cells.
  • The protective effects of CTRP3 are mediated through the activation of the PI3K/Akt/eNOS signaling pathway.
  • CTRP3 represents a promising therapeutic candidate for atherosclerosis treatment.
Keywords:
CTRP3PI3K/Akt/eNOS pathwayendothelial functioninflammatory responseox-LDL

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