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Endothelial dysfunction, hemodynamic forces, and atherogenesis.

M A Gimbrone1, J N Topper, T Nagel

  • 1Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115-5817, USA. mgimbrone@rics.bwh.harvard.edu

Annals of the New York Academy of Sciences
|June 24, 2000
PubMed
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Hemodynamic forces influence atherosclerosis by regulating endothelial genes. Specific shear stresses activate protective genes, potentially preventing lesion formation in arteries.

Area of Science:

  • Cardiovascular Biology
  • Translational Medicine
  • Biophysics

Background:

  • Endothelial dysfunction contributes to atherosclerosis pathogenesis.
  • Atherosclerotic lesions often localize to areas with disturbed blood flow patterns.
  • The vascular endothelium senses and responds to hemodynamic forces from pulsatile blood flow.

Purpose of the Study:

  • To investigate how hemodynamic forces regulate endothelial gene expression.
  • To explore the role of specific shear stress patterns in atherogenesis.
  • To identify endothelial genes involved in atheroprotection.

Main Methods:

  • Analysis of gene regulation by transcription factors (NF kappa B, Egr-1) and shear-stress response elements (SSREs).
  • Comparison of gene expression patterns under steady laminar versus non-laminar shear stress.

Related Experiment Videos

  • Examination of endothelial response to cytokine stimulation (e.g., IL-1 beta).

    • Main Results:

    • Steady laminar shear stress upregulates atheroprotective genes like eNOS, COX-2, and Mn-SOD.
    • Distinct gene expression patterns are induced by different shear stress types and cytokine stimulation.
    • Transcription factors bind to SSREs in biomechanically inducible genes.

    Conclusions:

    • Hemodynamic forces selectively regulate endothelial gene expression.
    • Upregulation of atheroprotective genes by laminar shear stress may prevent lesion formation.
    • Endothelial response to mechanical forces is a key factor in atherosclerosis development.