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Results In human microvascular endothelial cells (HMEC), TRPC4 was found to co-precipitate with VE-cadherin, indicating a physical coupling between TRPC4 and components of junctional complexes. Membrane presentation of TRPC4 as determined by surface biotinylation was found dependent on the formation of cell-cell contacts. Membrane presentation of TRPC4 was divergently affected by pro-inflammatory stimuli in cell displaying cell-cell contacts as compared to cells lacking contacts. At >90% confluency, epidermal growth factor (EGF) reduced membrane presentation of both VE-cadherin and TRPC4. By contrast, enhanced EGF-induced surface recruitment of TRPC4 was observed when cell-cell contacts were lacking. Cell adhesion-dependent targeting of TRPC4 was further analyzed by fluorescence imaging of channel localization and cellular Ca2+ signals in HMEC as well as in HEK293 expression system. Conclusion Our results suggest recruitment of TRPC4 into a junctional signaling microdomain of the vascular endothelium.

Cell adhesion-dependent trafficking and targeting of TRPC4 channels in human vascular endothelium