CTRP13 inhibits atherosclerosis via autophagylysosome-dependent degradation of CD36

Cheng Wang, Wenjing Xu, Minglu Liang, Dan Huang, Kai Huang

Research output: Contribution to journalArticle

12 Scopus citations

Abstract

C1q/tumor necrosis factor-related protein 13 (CTRP13) is a secreted adipokine that can ameliorate abnormalglucose andlipidmetabolism.However, the functional role ofCTRP13 inthedevelopment of atherosclerotic plaques has yet to be described. In this study,we collected blood samples frompatients of coronary artery diseases and apolipoproteinE (ApoE)2/2 mice thatwere fedaWestern diet for 12wkto induce atherosclerosis and found that serum CTRP13 level was decreased. En face staining of aortas and aortic sinus inApoE2/2mice showed that ectopic CTRP13 infusion in vivo dramatically decreased lesion areas, as well as reduced inflammatory responseswith less macrophage content. In primary peritoneal macrophages in vitro, CTRP13 supplement reduced oxidized LDL uptake, foam-cell formation, and trapping, togetherwith the suppressed cluster of differentiation 36 (CD36) protein levels. Reduced CD36 protein level was attributed to the autophagy-lysosome-dependent degradation of CD36 at the post-transcriptional level. The blocking of autophagy-lysosome induction could increase CD36 protein level, foam-cell formation, and migration, thus abolishing the protective effects of CTRP13 on atherosclerosis. In summary, these findings define CTRP13 as a novel approach for preventing atherosclerotic plaque formation via modulation of lipid uptake and foam-cellmigration.

Original languageEnglish (US)
Pages (from-to)2290-2300
Number of pages11
JournalFASEB Journal
Volume33
Issue number2
DOIs
StatePublished - 2019

Keywords

  • Lipid uptake
  • Macrophage
  • Post-transcriptional
  • Trapping

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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