Details

Autor(en) / Beteiligte

• Ma, Xin
• Cheng, Kwong-Tai
• Wong, Ching-On
• O’Neil, Roger G
• Birnbaumer, Lutz
• Ambudkar, Indu S
• Yao, Xiaoqiang

Titel

Heteromeric TRPV4-C1 channels contribute to store-operated Ca2+ entry in vascular endothelial cells

Ist Teil von

• Cell calcium (Edinburgh), 2011-12, Vol.50 (6), p.502-509

Erscheinungsjahr

2011

Link zum Volltext

Quelle

Elsevier ScienceDirect Journals Complete

Beschreibungen/Notizen

• Abstract 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.