What question did this study set out to answer?

Characterize the biological mechanisms by which vascular endothelial cells distinguish and respond to hemodynamic shear stress versus cyclical strain under acute and chronic conditions.

September 1, 1998Kidney InternationalOpen Access

Shear stress and the endothelium

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Authors

BBBarbara J. BallermannUniversity of Alberta ADAlan DardikIcahn School of Medicine at Mount Sinai EEEudora EngNorthwestern University

Discussion

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Implication

Mechanistic review reveals distinct endothelial adaptations to acute and chronic shear stress in vascular cells, highlighting bioengineering applications for durable artificial vascular grafts.

Key Points

Characterize the biological mechanisms by which vascular endothelial cells distinguish and respond to hemodynamic shear stress versus cyclical strain under acute and chronic conditions.
Evaluated in vitro signaling pathways, transcription factor activation, and gene transcription profiles in endothelial cells exposed to acute shear stress.
Analyzed structural remodeling, cellular adhesion, and monolayer retention of endothelial cells subjected to chronic shear stress in vascular graft models.
Acute shear stress induces rapid cytoskeletal remodeling, triggers nitric oxide and prostacyclin release, and activates transcription factors (NF-kappaB, c-fos, c-jun, SP-1) and inflammatory-like genes.
Chronic shear stress drives endothelial cell flattening, promotes cellular differentiation, and markedly increases substratum adhesion, enabling the stable retention of endothelial monolayers on implanted vascular prostheses.

Cite This Study

Ballermann et al. (1998) studied this question.

synapsesocial.com/papers/6aa2fe2421270d8a3eea5059 https://doi.org/10.1046/j.1523-1755.1998.06720.x

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September 1, 1998Kidney InternationalOpen Access

Shear stress and the endothelium

View Full Paper

Ask AI

Bookmark

Authors

BBBarbara J. BallermannUniversity of Alberta ADAlan DardikIcahn School of Medicine at Mount Sinai EEEudora EngNorthwestern University

Discussion

Member takes

Implication

Mechanistic review reveals distinct endothelial adaptations to acute and chronic shear stress in vascular cells, highlighting bioengineering applications for durable artificial vascular grafts.

Key Points

Characterize the biological mechanisms by which vascular endothelial cells distinguish and respond to hemodynamic shear stress versus cyclical strain under acute and chronic conditions.
Evaluated in vitro signaling pathways, transcription factor activation, and gene transcription profiles in endothelial cells exposed to acute shear stress.
Analyzed structural remodeling, cellular adhesion, and monolayer retention of endothelial cells subjected to chronic shear stress in vascular graft models.
Acute shear stress induces rapid cytoskeletal remodeling, triggers nitric oxide and prostacyclin release, and activates transcription factors (NF-kappaB, c-fos, c-jun, SP-1) and inflammatory-like genes.
Chronic shear stress drives endothelial cell flattening, promotes cellular differentiation, and markedly increases substratum adhesion, enabling the stable retention of endothelial monolayers on implanted vascular prostheses.

Cite This Study

Ballermann et al. (1998) studied this question.

synapsesocial.com/papers/6aa2fe2421270d8a3eea5059 https://doi.org/10.1046/j.1523-1755.1998.06720.x

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