Role of caveolin-1 in the regulation of the vascular shear stress response
Philippe G. Frank, Michael P. Lisanti
Philippe G. Frank, Michael P. Lisanti
Published May 1, 2006
Citation Information: J Clin Invest. 2006;116(5):1222-1225. https://doi.org/10.1172/JCI28509.
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Commentary

Role of caveolin-1 in the regulation of the vascular shear stress response

Abstract

In blood vessels, endothelia are submitted to constant shear effects and are, under normal conditions, capable of responding to any variation in hemodynamic forces. Caveolae — 50- to 100-nm plasma membrane invaginations present at the surface of terminally differentiated cells and particularly enriched in ECs — are composed of a high sphingolipid and cholesterol content and the protein caveolin-1 (Cav-1). Previous studies have suggested that caveolae and endothelial Cav-1 may regulate the vascular response to altered shear stress. In this issue of the JCI, Yu et al. have examined the role of Cav-1/caveolae in the regulation of flow-induced alterations (i.e., mechanotransduction) in vessels from wild-type mice, Cav-1–deficient mice, and Cav-1–deficient mice re-expressing Cav-1 only in ECs. Their data suggest that caveolae/Cav-1 may act as sensors of altered shear stress and that they also organize the signaling response in stimulated ECs (see the related article beginning on page 1284).

Authors

Philippe G. Frank, Michael P. Lisanti

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Figure 1

Cav-1 deficiency is associated with an altered response to modified shear stress conditions.

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Cav-1 deficiency is associated with an altered response to modified shea...
In this issue of the JCI, Yu et al. (20) have demonstrated that Cav-1 deficiency is associated with a reduced vascular response upon the alteration of shear stress conditions. Accordingly, reduced blood flow in the common carotid artery (due to ligation) was associated with reduced vessel lumen diameter in the case of wild-type animals. However, in Cav-1 KO mice, increased SMC proliferation was detected in the media but no change in the vessel lumen diameter was observed. Re-expression of Cav-1 in ECs alone was sufficient to eliminate this phenotype in Cav-1 KO mice.