Genetic evidence supporting caveolae microdomain regulation of calcium entry in endothelial cells.
Various cellular signals initiate calcium entry into cells, and there is evidence that lipid rafts and caveolae may concentrate proteins that regulate transmembrane calcium fluxes. Here, using mice deficient in caveolin-1 (Cav-1) and Cav-1 knock-out reconstituted with endothelium-specific Cav-1, we show that Cav-1 is essential for calcium entry in endothelial cells and governs the localization and protein-protein interactions between transient receptor channels C4 and C1. Thus, Cav-1 is required for calcium entry in vascular endothelial cells and perhaps other specialized cell types containing caveolae.
Murata
Takahisa
T
Department of Pharmacology and Program in Vascular Cell Signaling and Therapeutics, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06536, USA.
Lin
Michelle I
MI
Stan
Radu V
RV
Bauer
Phillip Michael
PM
Yu
Jun
J
Sessa
William C
WC
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D021941:Caveolae / Q000378:metabolism*; D051242:Caveolin 1 / Q000235:genetics / Q000378:metabolism*; D042783:Endothelial Cells / Q000378:metabolism* / Q000648:ultrastructure; D017136:Ion Transport / Q000235:genetics; D051379:Mice; D018345:Mice, Knockout; D050052:TRPC Cation Channels / Q000378:metabolism*
D051242:Caveolin 1; D050052:TRPC Cation Channels; C489571:TRPC4 ion channel; C096351:transient receptor potential cation channel, subfamily C, member 1; D002118:Calcium