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Published on: June 11, 2017
Vascular endothelial cell activation in models of vascular and glomerular injury
1Renal Division, St. Michael's Hospital, Toronto, Ontario, Canada.
Activated vascular endothelium evidences a diverse array of responses to biochemical and physical stimuli with modulating effects on leukocyte trafficking, vascular permeability and vasomotor tone controlling microvascular blood flow. Clearly, glomerular endothelial cells share in common with large-vessel endothelium some components of the cytokine-activated phenotype. These findings provide insight into mechanisms of glomerular injury. Speculation about potentially unique aspects of microvascular regulation which might be important in glomerular injury suggests that novel aspects of cytokine-activation may be evident in microvascular endothelial cells. Molecular mechanisms underlying signal transduction of stimulus-induced alterations in endothelial phenotype implicate cis-regulatory processes that are unique in diversity and expression. Further elucidation of these mechanisms may suggest interventions directed towards inhibiting the pathophysiologic sequelae of endothelial cell activation.
Activated vascular endothelium evidences a diverse array of responses to biochemical and physical stimuli with modulating effects on leukocyte trafficking, vascular permeability and vasomotor tone controlling microvascular blood flow. Clearly, glomerular endothelial cells share in common with large-vessel endothelium some components of the cytokine-activated phenotype. These findings provide insight into mechanisms of glomerular injury. Speculation about potentially unique aspects of microvascular regulation which might be important in glomerular injury suggests that novel aspects of cytokine-activation may be evident in microvascular endothelial cells. Molecular mechanisms underlying signal transduction of stimulus-induced alterations in endothelial phenotype implicate cis-regulatory processes that are unique in diversity and expression. Further elucidation of these mechanisms may suggest interventions directed towards inhibiting the pathophysiologic sequelae of endothelial cell activation.

