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NDRG2 induced by oxidized LDL in macrophages antagonizes growth factor productions via selectively inhibiting ERK

Shumei Liu1, Pengyuan Yang, Hui Kang

  • 1Department of Pharmacology & School of Pharmacy, Second Military Medical University, Shanghai 200433, PR China.

Biochimica Et Biophysica Acta
|October 10, 2009
PubMed

Insights

N-Myc downstream-regulated protein 2 (NDRG2) is a novel marker in atherosclerosis. NDRG2 negatively regulates growth factors, impacting vascular smooth muscle cell proliferation and offering potential therapeutic targets.

Area of Science:

  • Cardiovascular Biology
  • Cellular and Molecular Medicine
  • Inflammation Research

Background:

  • Macrophage foam cells are key in atherogenesis, releasing inflammatory mediators.
  • Oxidized low-density lipoprotein (oxLDL) triggers macrophage activation, contributing to plaque development.

Purpose of the Study:

  • To identify and characterize a novel protein marker involved in macrophage activation during atherogenesis.
  • To elucidate the regulatory role of NDRG2 in growth factor production and vascular smooth muscle cell proliferation.

Main Methods:

  • Quantitative analysis of NDRG2 expression in macrophages and human atherosclerotic plaques.
  • Over-expression and siRNA knockdown of NDRG2 in macrophages.
  • Assessment of platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) production.
  • Investigation of MAPK signaling pathways (ERK1/2, P38, JNK1/2).
  • Vascular smooth muscle cell (VSMC) proliferation assays and antibody neutralization studies.

Main Results:

  • NDRG2 expression is significantly increased in oxLDL-treated macrophages and human atherosclerotic plaques.
  • NDRG2 acts as a negative regulator of PDGF and VEGF production in macrophages.
  • ERK1/2 activation mediates NDRG2's regulation of PDGF and VEGF.
  • Modulation of NDRG2 affects macrophage-conditioned medium-induced VSMC proliferation, which is partially mediated by PDGF.

Conclusions:

  • NDRG2 is implicated in oxLDL-induced macrophage activation and atherogenesis.
  • NDRG2 influences VSMC proliferation via regulation of PDGF and VEGF through the ERK1/2 pathway.
  • NDRG2 represents a potential therapeutic target for treating atherosclerosis.

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