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Related Experiment Videos

Control of endothelial cell gene expression by flow

A M Malek1, S Izumo

  • 1Department of Neurosurgery, Harvard Medical School, Boston, MA 02215, USA. ammalek@bics.bwh.harvard.edu

Journal of Biomechanics
|December 1, 1995
PubMed
Summary

Fluid shear stress dynamically regulates endothelial cell gene expression, influencing vessel health. This response is shear stress-dependent, not shear rate-dependent, impacting vascular remodeling and atherosclerosis.

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Area of Science:

  • Cardiovascular Biology
  • Endothelial Cell Biology
  • Hemodynamics

Background:

  • The vessel wall responds to hemodynamic forces like pressure and flow.
  • Endothelial cells at the blood-vessel interface are key regulators of vascular structure and function.
  • Understanding endothelial response to shear stress is crucial for vascular health.

Purpose of the Study:

  • To investigate how fluid shear stress affects endothelial cell gene expression.
  • To characterize the patterns and mechanisms of endothelial response to shear stress.
  • To explore the implications for vascular remodeling and atherosclerosis.

Main Methods:

  • Utilized bovine aortic endothelium monolayers.
  • Applied controlled fluid shear stress.

Related Experiment Videos

  • Analyzed differential regulation of endothelial-derived products and mRNA levels.
  • Investigated shear stress vs. shear rate dependency using dextran supplementation.

    • Main Results:

    • Fluid shear stress induces simultaneous, differential regulation of endothelial products.
    • Downregulation of endothelin-1 mRNA by flow is reversible and shear stress-dependent.
    • Endothelial gene expression responses to shear stress were classified into three patterns: transient (Type I), sustained (Type II), and biphasic (Type III).

    Conclusions:

    • Endothelial cell phenotype is exquisitely modulated by local fluid shear stress.
    • Mechanisms involve shear stress response elements (SSRE).
    • Findings offer insights into flow-dependent vascular remodeling and atherosclerosis development in low shear stress areas.