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C1q/TNF-Related Protein 9 Inhibits THP-1 Macrophage Foam Cell Formation by Enhancing Autophagy

Lu Zhang1,2, Qi Liu1,2, Hui Zhang3

  • 1Department of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.

Journal of Cardiovascular Pharmacology
|July 7, 2018
PubMed

Insights

C1q/tumor necrosis factor-related protein-9 (CTRP9) reduces lipid accumulation in macrophages, preventing foam cell formation. This adipokine promotes cholesterol efflux and enhances autophagy via the AMPK/mTOR pathway, offering a protective effect against atherosclerosis.

Area of Science:

  • Cardiovascular Biology
  • Cellular Metabolism
  • Molecular Medicine

Background:

  • Atherosclerosis pathogenesis involves lipid-laden macrophages and foam cell formation.
  • C1q/tumor necrosis factor-related protein-9 (CTRP9) is a novel adipokine with known cardiovascular benefits.
  • The role of CTRP9 in oxidized low-density lipoprotein (ox-LDL)-induced foam cell formation remains uninvestigated.

Purpose of the Study:

  • To investigate the effect of CTRP9 on ox-LDL-induced foam cell formation in macrophages.
  • To elucidate the underlying mechanisms, including cholesterol metabolism and autophagy, involved in CTRP9's action.

Main Methods:

  • THP-1 macrophages were treated with ox-LDL and CTRP9.
  • Lipid droplet quantification, cholesteryl ester (CE) level measurement, and cholesterol efflux assays were performed.
  • Autophagy markers (LC3 II, p62) and signaling pathways (AMPK/mTOR) were analyzed.
  • Inhibitors of autophagy (3-methyladenine) and AMPK (Compound C) were used to confirm mechanisms.

Main Results:

  • CTRP9 significantly reduced lipid droplets and CE levels in ox-LDL-treated macrophages.
  • CTRP9 promoted cholesterol efflux and increased expression of ABCA1 and ABCG1.
  • CTRP9 enhanced autophagy, evidenced by increased LC3 II and decreased p62.
  • Inhibition of autophagy or the AMPK/mTOR pathway abolished CTRP9's protective effects.

Conclusions:

  • CTRP9 protects against atherosclerosis by inhibiting foam cell formation.
  • CTRP9 promotes cholesterol efflux and enhances autophagy through the AMPK/mTOR signaling pathway.
  • CTRP9 represents a potential therapeutic target for atherosclerosis treatment.

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