کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2166106 | 1549322 | 2011 | 8 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Heteromeric TRPV4-C1 channels contribute to store-operated Ca2+ entry in vascular endothelial cells Heteromeric TRPV4-C1 channels contribute to store-operated Ca2+ entry in vascular endothelial cells](/preview/png/2166106.png)
There is controversy as to whether TRP channels participate in mediating store-operated current (ISOC) and store-operated Ca2+ entry (SOCE). Our recent study has demonstrated that TRPC1 forms heteromeric channels with TRPV4 in vascular endothelial cells and that Ca2+ store depletion enhances the vesicle trafficking of heteromeric TRPV4-C1 channels, causing insertion of more channels into the plasma membrane in vascular endothelial cells. In the present study, we determined whether the enhanced TRPV4-C1 insertion to the plasma membrane could contribute to SOCE and ISOC. We found that thapsigargin-induced SOCE was much lower in aortic endothelial cells derived from trpv4−/− or trpc1−/− knockout mice when compared to that of wild-type mice. In human umbilical vein endothelial cells (HUVECs), thapsigargin-induced SOCE was markedly reduced by knocking down the expression of TRPC1 and/or TRPV4 with respective siRNAs. Brefeldin A, a blocker of vesicular translocation, inhibited the SOCE. These results suggest that an enhanced vesicular trafficking of heteromeric TRPV4-C1 channels contributes to SOCE in vascular endothelial cells. Vascular tension studies suggest that such an enhanced trafficking of TRPV4-C1 channels may play a role in thapsigargin-induced vascular relaxation in rat small mesenteric arteries.
Journal: Cell Calcium - Volume 50, Issue 6, December 2011, Pages 502–509