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Macrophage inflammatory protein-1beta induced cell adhesion with increased intracellular reactive oxygen species

Yuji Tatara1, Mitsuru Ohishi, Koichi Yamamoto

  • 1Department of Geriatric Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan.

Journal of Molecular and Cellular Cardiology
|March 31, 2009
PubMed
Abstract

Insights

Macrophage inflammatory protein-1 beta (MIP-1beta) promotes atherosclerosis by increasing cell adhesion and oxidative stress. Elevated MIP-1beta levels predict a higher risk of stroke and cardiovascular events in hypertensive patients.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Atherosclerosis involves monocyte adhesion to endothelium, mediated by inflammatory signals.
  • Reactive oxygen species (ROS) play a critical role in the pathogenesis of atherosclerosis.
  • Macrophage inflammatory protein-1 beta (MIP-1beta) is implicated in inflammatory processes.

Purpose of the Study:

  • To investigate the role of MIP-1beta in monocyte-endothelial cell adhesion and ROS production in vitro.
  • To determine if MIP-1beta can predict stroke and cardiovascular events in hypertensive patients.

Main Methods:

  • In vitro study using THP-1 cells and human umbilical vein endothelial cells stimulated with MIP-1beta or Angiotensin II (AngII).
  • Assessed ROS production, cell adhesion, and the effects of inhibitors targeting ROS signaling, PI3Kgamma, and Rac1.
  • Investigated the role of integrins VLA-4 and LFA-1 in cell adhesion.
  • Clinical study analyzing serum MIP-1beta levels as a predictor of cardiovascular events in hypertensive patients.

Main Results:

  • MIP-1beta and AngII significantly increased ROS production and THP-1 cell adhesion to endothelial cells.
  • Inhibition of ROS, PI3Kgamma, or Rac1, and treatment with fluvastatin, reduced MIP-1beta-induced cell adhesion and ROS production.
  • MIP-1beta stimulation did not alter surface expression of VLA-4 and LFA-1, but antibodies against these integrins reduced cell adhesion.
  • Elevated MIP-1beta levels were associated with an increased risk of stroke and cardiovascular events in hypertensive patients.

Conclusions:

  • MIP-1beta directly induces monocyte adhesion to endothelial cells via oxidative stress mediated by PI3k-Rac1 signaling pathways.
  • Serum MIP-1beta levels may serve as a valuable prognostic biomarker for cerebro-cardiovascular events in hypertensive individuals.

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