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Jun N-terminal kinase inhibitor blocks angiogenesis by blocking VEGF secretion and an MMP pathway

Shin-ichiro Miura1, Yoshino Matsuo, Keijiro Saku

  • 1Department of Cardiology, Fukuoka University School of Medicine, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, Japan. miuras@cis.fukuoka-u.ac.jp

Journal of Atherosclerosis and Thrombosis
|April 4, 2008
PubMed
Abstract

Insights

A Jun N-terminal kinase inhibitor (JNK-I) directly reduces vascular smooth muscle cell proliferation and endothelial cell tube formation, suggesting an anti-atherogenic effect. This occurs by decreasing vascular endothelial growth factor release from smooth muscle cells.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Atherosclerosis Research

Background:

  • Vascular smooth muscle cell (SMC) proliferation and endothelial cell (EC) angiogenesis are key in atherosclerotic plaque development.
  • The role of Jun N-terminal kinase (JNK) in atherosclerosis remains uncertain.

Purpose of the Study:

  • To investigate the direct impact of a JNK inhibitor (JNK-I) on human coronary SMC and EC functions.
  • To determine if JNK signaling is a viable target for anti-atherogenic therapies.

Main Methods:

  • Assessing the effects of JNK-I on SMC proliferation and EC tube formation in vitro.
  • Analyzing vascular endothelial growth factor (VEGF) levels in response to JNK-I treatment.
  • Evaluating the expression of pro-matrix metalloproteinase-2 in ECs.

Main Results:

  • JNK-I treatment of SMCs inhibited EC tube formation, mediated by reduced VEGF secretion.
  • JNK-I also decreased pro-matrix metalloproteinase-2 expression in ECs.
  • Reintroducing VEGF reversed the inhibitory effect of JNK-I on EC tube formation.

Conclusions:

  • JNK inhibition demonstrates a direct anti-atherogenic effect on both SMCs and ECs.
  • Targeting JNK signaling may offer a therapeutic strategy for preventing or treating atherosclerosis.

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