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Production of Nurr-1 Specific Polyclonal Antibodies Free of Cross-reactivity Against Its Close Homologs, Nor1 and Nur77
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Production of Nurr-1 Specific Polyclonal Antibodies Free of Cross-reactivity Against Its Close Homologs, Nor1 and Nur77

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Regulation of vascular smooth muscle cell proliferation by nuclear orphan receptor Nur77

Liyue Wang1, Fan Gong, Xiaoyan Dong

  • 1Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No 1277 Jiefang Avenue, Wuhan, 430020 Hubei, China.

Molecular and Cellular Biochemistry
|April 23, 2010
PubMed

Insights

Nur77 promotes vascular smooth muscle cell proliferation in arteriosclerosis. Atorvastatin down-regulates Nur77, suggesting a new therapeutic strategy for preventing artery narrowing by inhibiting cell growth.

Area of Science:

  • Vascular Biology
  • Molecular Medicine
  • Pharmacology

Background:

  • Nur77 is implicated in arteriosclerosis, with reported dual effects on vascular smooth muscle cell (VSMC) proliferation.
  • Platelet-derived growth factor (PDGF) is a key mediator of VSMC proliferation in atherogenesis and restenosis.

Purpose of the Study:

  • To investigate the role of Nur77 in VSMC proliferation.
  • To examine the effect of atorvastatin on Nur77 expression in VSMCs and in a rat restenosis model.

Main Methods:

  • Cellular models of VSMC proliferation induced by PDGF-B.
  • Rat carotid artery restenosis model.
  • Immunohistochemistry, RT-PCR, and Western blot analysis to assess Nur77 expression.
  • ERK-MAPK signaling pathway analysis.

Main Results:

  • PDGF-B upregulated Nur77 mRNA and protein expression in VSMCs via ERK-MAPK signaling.
  • Atorvastatin attenuated PDGF-B-induced Nur77 expression in VSMCs.
  • In the rat model, Nur77 was upregulated in neointima and downregulated by atorvastatin treatment.

Conclusions:

  • Nur77 promotes VSMC proliferation, contributing to arteriosclerosis.
  • Atorvastatin's downregulation of Nur77 offers a potential therapeutic strategy for atherogenesis by suppressing VSMC proliferation.

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