Abstract
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.
Highlights
The generation of receptor-induced cytosolic calcium signals involves the rapid, transient release of calcium from stores, mainly located in the endoplasmic reticulum (ER)2 followed by sustained entry of extracellular calcium [1]
TRPC1 was characterized as a component of SOC in nerve cells [8], subsequent studies indicated that TRPC3, TRPC4, and TRPC5 might contribute to calcium entry mechanisms after agonist stimulation (9 –11)
Cav-1 Is Necessary for Acetylcholine-induced Calcium Fluxes and Prostacyclin Production—Previously, we have established mice deficient in Cav-1 that were bred to transgenic mice expressing Cav-1 in endothelial cells only [23]
Summary
Generation of Cav-1-deficient and Endothelium-specific Cav-1 Transgenic Reconstituted (Cav-1 RC) Animals. Male mice (8 –10 weeks old) were used for the experiments
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