TRPC1 expression and distribution in rat hearts

Abstract

Transient receptor potential canonical (TRPC) proteins have been identified as a family of plasma membrane calcium-permeable channels. TRPC proteins can be activated by various stimuli and act as cellular sensors in mammals. Stretch-activated ion channels (SACs) have been proposed to underlie cardiac mechano-electric feedback (MEF), although the molecular entity of SAC remains unknown. There is evidence suggesting that transient receptor potential canonical 1 (TRPC1) is a stretch-activated ion channel. As a non-selective cation channel, TRPC1 may cause stretch-induced depolarization and arrhythmia and thus may contribute to the MEF of the heart. In this study, we examined the expression patterns of TRPC1 in detail at both the mRNA and protein levels in rat hearts. We isolated total RNA from the left and right atria, and the left and right ventricles, and detected TRPC1 mRNA in these tissues using reverse-transcriptase polymerase chain reaction (RT-PCR). To study the protein localization and targeting, we performed immunohistochemistry and immunofluorescence labeling with the antibody against TRPC1. TRPC1 was detected in the cardiomyocytes of the ventricle and atrium at both the mRNA and protein levels. The cell membrane and Ttubule showed strong fluorescence labeling in the ventricular myocytes. Purkinje cells, the endothelial cells and smooth muscle cells of the coronary arterioles also displayed TRPC1 labeling. No TRPC1 was detected in fibroblasts. In conclusion, TRPC1 is widely expressed in the rat heart, including in working cells, Purkinje cells and vascular cells, suggesting that it plays an important role in the heart. The specific distribution pattern offered a useful insight into its function in adult rat ventricular cells. Further investigations are needed to clarify the role of TRPC1 in regulating cardiac activity, including cardiac MEF.

Transcriptomic profile of the mechanosensitive ion channelome in human cardiac fibroblasts

“…86 Among all TRPC channels expressed in cardiac tissue, only TRPC1 and TRPC6 exhibit mechanosensitivity. 86,87 Despite published data by Huang et al 88 that TRPC1 expression is not detected in HCFs; in this, study, we detected significant expression of TRPC1 (Figure 2(G)). Further studies have shown that TRPC6 exhibits mechanosensitivity upon activation, and it is postulated that the channel's involvement in the response to mechanical stimuli requires PLA2/-hydroxylase metabolite pathway (20-HETE pathway) activation.…”

TRPC channels: Dysregulation and Ca²⁺ Mishandling In Ischemic Heart Disease

“…In human cardiac tissues and/or neonatal rat cardiomyocytes mRNA of TRPC5 [20,21] and TRPC6 [22] were detected. In animal model, the expression of TRPC1/3-7 have been confirmed in adult rat and mouse ventricle and atrial cardiac myocytes either at mRNA or protein levels [13,23,24]. Others reports showed that TRPC1/3-6 are expressed in rat ventricular myocytes of fetal and neonatal ventricular myocytes [19,25].…”

Active force generation contributes to the complexity of spontaneous activity and to the response to stretch of murine cardiomyocyte cultures

“…The modulation of electrophysiological characteristics by mechanical influences is generally known as mechano-electrical feedback (MEF; Kamkin et al, 2005;Kohl et al, 1994Kohl et al, , 2006McNary et al, 2008;Quinn et al, 2014;Riemer & Tung, 2003). Mechano-electrical feedback is most frequently attributed to non-selective SACs (Huang et al, 2009;McNary et al, 2008), which cause depolarization and triggered activity when activated during diastole (Quinn et al, 2017;Riemer & Tung, 2003). Stretch-activated channels can be present constitutively in cardiomyocytes or in fibroblasts electrically coupled to myocytes (Grand et al, 2014;Kohl et al, 1994;Quinn et al, 2014).…”