Expression and relative abundance of short transient receptor potential channels in the rat renal microcirculation

Abstract

Facemire, Carie S., Peter J. Mohler, and William J. Arendshorst. Expression and relative abundance of short transient receptor potential channels in the rat renal microcirculation. Am J Physiol Renal Physiol 286: F546-F551, 2004. First published December 16, 2004; 10.1152/ajprenal.00338.2003In the resistance vessels of the renal microcirculation, store-and/or receptor-operated calcium entry contribute to the rise in vascular smooth muscle cell (VSMC) intracellular calcium concentration in response to vasoconstrictor hormones. Short transient receptor potential (TRPC) channels are widely expressed in mammalian tissues and are proposed mediators of voltage-independent cation entry in multiple cell types, including VSMCs. The seven members of the TRPC gene family (TRPC1-7) encode subunit proteins that are thought to form homo-and heterotetrameric channels that are differentially regulated depending on their subunit composition. In the present study, we demonstrate the relative abundance of TRPC mRNA and protein in freshly isolated rat renal resistance vessels, glomeruli, and aorta. TRPC1, 3, 4, 5, and 6 mRNA and protein were detected in both renal resistance vessels and aorta, whereas TRPC2 and TRPC7 mRNA were not expressed. TRPC1, 3, 5, and 6 protein was present in glomeruli. TRPC3 and TRPC6 protein levels were significantly greater in the renal resistance vessels, about six-to eightfold higher than in aorta. These data suggest that TRPC3 and TRPC6 may play a role in mediating voltage-independent calcium entry in renal resistance vessels that is functionally distinct from that in aorta. vascular smooth muscle cells; resistance vessels; aorta; store-operated channel; receptor-operated channel ALTHOUGH L-TYPE VOLTAGE-DEPENDENT calcium channels have been the focus of much study on the regulation of vascular reactivity, voltage-independent cation channels represent an important component of calcium entry in cells of the systemic and renal vasculature as well. In the preglomerular resistance vessels (interlobular arteries and afferent arterioles), non-Ltype calcium entry contributes to vascular smooth muscle cell (VSMC) calcium responses to norepinephrine (6, 27) and vasopressin (8), vasoactive hormones that regulate renal blood flow and glomerular filtration rate. Store-operated calcium influx has been shown to negatively regulate renin secretion by juxtaglomerular cells (28). In VSMCs of conduit arteries such as aorta, calcium entry through store-and/or receptor-operated channels (SOCs, ROCs) is activated by norepinephrine and endothelin-1 (10,30,38). Calcium entry through these SOCs and ROCs also modulates vascular endothelial and glomerular mesangial cell function (20,24,26). These receptor-mediated calcium entry pathways have been incompletely characterized due to a lack of pharmacological agents able to discriminate between the function of SOCs and ROCs. Identification of the molecular components of these cation channels in renal resistance vessels would permit genetic manipulation and more detailed investigatio...

Expression and distribution of transient receptor potential (TRP) channels in bladder epithelium

“…TRPC4 has four protein variants, with the full-length species containing 974 amino acids and a predicted molecular mass of ϳ112 kDa. The protein species we observed is likely to be a variant that contains 564 amino acids and has been reported previously (19). The anti-TRPV1 antibody weakly detected a protein species of 75 kDa, and this binding was abolished by the control peptide (Fig.…”

Attenuated mesangial cell proliferation related to store-operated Ca2+ entry in aged rat: the role of STIM 1 and Orai 1

“…TRPC1, TRPC3, TRPC4, TRPC5, and TRPC6 proteins were identified in GMCs (Facemire et al 2004;Sours-Brothers et al 2009). Previous studies demonstrated that TRPC1, 4, and 6 contributed to SOCE in GMCs (Sours-Brothers et al 2009;Wang et al 2004Wang et al , 2007.…”

Evidence of a Role for Fibroblast Transient Receptor Potential Canonical 3 Ca2+ Channel in Renal Fibrosis

“…44,45 Few other studies reported the presence of TRPC channels in normal rat kidney cell lines 46,47 and identified their localization in the adult rat and human kidney. [48][49][50][51] TRPC3 is also responsible for transepithelial Ca 2+ flux in principal cells of the renal collecting duct [52][53][54] ; however, a clear functional in vivo role of such channels remains totally unclear, especially in the diseased kidney. Therefore, it is important to study the role of TRPC3 in renal fibroblasts and its role in the pathogenesis of renal fibrosis associated with kidney disease.…”