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lüll Functional role of vanilloid transient receptor potential 4-canonical transient receptor potential 1 complex in flow-induced Ca2+ influx Ma X; Qiu S; Luo J; Ma Y; Ngai CY; Shen B; Wong CO; Huang Y; Yao XArterioscler Thromb Vasc Biol 2010[Apr]; 30 (4): 851-8OBJECTIVE: The present study is aimed at investigating the interaction of TRPV4 with TRPC1 and the functional role of such an interaction in flow-induced Ca(2+) influx. Hemodynamic blood flow is an important physiological factor that modulates vascular tone. One critical early event in this process is a cytosolic Ca(2+) ([Ca(2+)](i)) rise in endothelial cells in response to flow. METHODS AND RESULTS: With the use of fluorescence resonance energy transfer, coimmunoprecipitation, and subcellular colocalization methods, it was found that TRPC1 interacts physically with TRPV4 to form a complex. In functional studies, flow elicited a transient [Ca(2+)](i) increase in TRPV4-expressing human embryonic kidney (HEK) 293 cells. Coexpression of TRPC1 with TRPV4 markedly prolonged this [Ca(2+)](i) transient; it also enabled this [Ca(2+)](i) transient to be negatively modulated by protein kinase G. Furthermore, this flow-induced [Ca(2+)](i) increase was markedly inhibited by anti-TRPC1-blocking antibody T1E3 and a dominant-negative construct TRPC1 Delta 567-793 in TRPV4-C1-coexpressing HEK cells and human umbilical vein endothelial cells. T1E3 also inhibited flow-induced vascular dilation in isolated rat small mesenteric artery segments. CONCLUSIONS: This study shows that TRPC1 interacts physically with TRPV4 to form a complex, and this TRPV4-C1 complex may mediate flow-induced Ca(2+) influx in vascular endothelial cells. The association of TRPC1 with TRPV4 prolongs the flow-induced [Ca(2+)](i) transient, and it also enables this [Ca(2+)](i) transient to be negatively modulated by protein kinase G. This TRPV4-C1 complex plays a key role in flow-induced endothelial Ca(2+) influx.|*Calcium Signaling/drug effects[MESH]|Animals[MESH]|Cells, Cultured[MESH]|Cyclic GMP-Dependent Protein Kinases/metabolism[MESH]|Endothelial Cells/drug effects/*metabolism[MESH]|Fluorescence Resonance Energy Transfer[MESH]|Humans[MESH]|Immunoprecipitation[MESH]|Kinetics[MESH]|Male[MESH]|Membrane Potentials[MESH]|Mesenteric Arteries/metabolism[MESH]|Microscopy, Fluorescence[MESH]|Multiprotein Complexes[MESH]|Mutation[MESH]|Patch-Clamp Techniques[MESH]|Phorbol Esters/pharmacology[MESH]|Protein Binding[MESH]|RNA Interference[MESH]|Rats[MESH]|Rats, Sprague-Dawley[MESH]|TRPC Cation Channels/genetics/*metabolism[MESH]|TRPV Cation Channels/agonists/genetics/*metabolism[MESH]|Transfection[MESH]|Vasodilation[MESH] |