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Updated: Aug 18, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

Transforming growth factor-beta1 (TGF-beta1) and TGF-beta2 decrease expression of CD36, the type B scavenger

J Han1, D P Hajjar, J M Tauras

  • 1Department of Pathology and Center of Vascular Biology, Weill Medical College of Cornell University, New York, New York 10021, USA.

The Journal of Biological Chemistry
|January 8, 2000
PubMed

Insights

Transforming growth factor-beta (TGF-beta) 1 and 2 reduce CD36 expression in macrophages. This occurs via a pathway involving mitogen-activated protein kinase (MAPK) and peroxisome proliferator-activated receptor gamma (PPAR-gamma) phosphorylation, impacting foam cell formation in atherosclerosis.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • CD36 is a scavenger receptor crucial for macrophage foam cell development in atherosclerosis.
  • CD36 expression is regulated by macrophage differentiation and soluble mediators.

Purpose of the Study:

  • To investigate the effects of transforming growth factor-beta1 (TGF-beta1) and TGF-beta2 on CD36 expression in macrophages.
  • To elucidate the molecular mechanisms underlying TGF-beta-mediated regulation of CD36.

Main Methods:

  • THP-1 macrophages were differentiated and treated with TGF-beta1, TGF-beta2, oxidized LDL, or PPAR-gamma ligands.
  • Expression of CD36 mRNA and surface protein was assessed.
  • Phosphorylation of MAP kinase and PPAR-gamma was analyzed.
  • The impact of MAP kinase inhibitors was evaluated.

Main Results:

  • TGF-beta1 and TGF-beta2 significantly decreased CD36 mRNA and protein expression.
  • TGF-beta suppressed CD36 induction by oxidized LDL and a PPAR-gamma ligand.
  • TGF-beta increased MAP kinase and PPAR-gamma phosphorylation.
  • MAP kinase inhibitors reversed TGF-beta's suppression of CD36 and PPAR-gamma phosphorylation.

Conclusions:

  • TGF-beta1 and TGF-beta2 down-regulate CD36 expression in macrophages.
  • This regulation involves MAP kinase activation and subsequent PPAR-gamma phosphorylation.
  • The findings reveal a novel mechanism for controlling CD36 transcription and its role in atherogenesis.

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