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Related Experiment Videos

Shear stress and the endothelium

B J Ballermann1, A Dardik, E Eng

  • 1Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. bjballer@welchlink.welch.jhu.edu

Kidney International. Supplement
|September 15, 1998
PubMed
Summary

Shear stress, a force from blood flow, rapidly alters endothelial cells (ECs) and gene expression. Chronic shear stress promotes EC adhesion and differentiation, aiding vascular graft development.

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Area of Science:

  • Cardiovascular Biology
  • Cellular Mechanotransduction
  • Endothelial Cell Biology

Background:

  • Vascular endothelial cells (ECs) are subjected to hemodynamic forces, including cyclical strain and shear stress.
  • Shear stress, a frictional force from blood flow, deforms ECs along the flow direction.
  • The EC response to shear stress is distinct from cyclical strain, indicating mechanisms beyond cytoskeletal strain alone.

Purpose of the Study:

  • To investigate the acute and chronic effects of shear stress on vascular endothelial cells (ECs).
  • To elucidate the molecular signaling pathways and gene expression changes induced by shear stress.
  • To explore the potential of shear stress-induced EC adaptations in vascular graft technology.

Main Methods:

  • In vitro exposure of ECs to acute and chronic shear stress.

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  • Analysis of cytoskeletal remodeling and signaling cascade activation.
  • Measurement of gene and protein expression, including inflammatory markers and growth factors.
  • Assessment of EC adhesion and differentiation under shear stress.

    • Main Results:

    • Acute shear stress triggers rapid EC cytoskeletal remodeling, signaling activation (NF-kappaB, c-fos, c-jun, SP-1), and release of nitric oxide and prostacyclin.
    • Transcriptional activation of genes such as ICAM-1, MCP-1, tissue factor, PDGF-B, TGF-beta1, cyclooxygenase-II, and eNOS occurs following acute shear stress.
    • Chronic shear stress induces EC structural remodeling, flattening, increased adhesion, and differentiation.
    • Enhanced EC adhesion under chronic shear stress facilitates the creation of confluent EC monolayers for vascular grafts.

    Conclusions:

    • Shear stress elicits complex and distinct responses in ECs, involving rapid signaling and gene expression changes, as well as adaptive structural remodeling.
    • The molecular responses to acute shear stress resemble those induced by inflammatory cytokines.
    • Chronic shear stress-induced EC adaptations, particularly increased adhesion, offer a promising strategy for improving vascular prostheses endothelialization.