Proteins have already been identified as a family of plasma membrane calcium-permeable channels. TRPC proteins is often activated by many stimuli and act as cellular sensors in mammals. Stretch-activated ion channels (SACs) have already been proposed to underlie cardiac mechano-electric feedback (MEF), even though the molecular entity of SAC remains unknown. There is evidence suggesting that transient receptor potential canonical 1 (TRPC1) is often a stretch-activated ion channel. As a non-selective cation channel, TRPC1 may perhaps bring about stretch-induced depolarization and arrhythmia and hence might contribute to the MEF on 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 in the left and suitable atria, and the left and proper 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 together with the antibody against TRPC1. TRPC1 was detected within the cardiomyocytes of your ventricle and atrium at each the mRNA and protein levels. The cell membrane and Ttubule showed powerful fluorescence labeling in the ventricular myocytes. Purkinje cells, the endothelial cells and smooth muscle cells in the coronary arterioles also displayed TRPC1 labeling. No TRPC1 was detected in fibroblasts. In conclusion, TRPC1 is widely expressed in the rat heart, which includes in working cells, Purkinje cells and vascular cells, suggesting that it plays an essential role within the heart. The certain distribution pattern presented a helpful insight into its function in adult rat ventricular cells. Additional investigations are necessary to clarify the function of TRPC1 in regulating cardiac activity, like cardiac MEF. Key words: TRPC1, Heart, Expression and distribution. Correspondence: Weizhen Niu, Department of physiology, Capital Health-related University, You An Males Wai Street Xitoutiao ten, Beijing 100069, China Tel: +86.10.83911470. E-mail: [email protected] accepted on September 9, 2009 European Journal of Histochemistry 2009; vol. 53 issue four (October-December): 217-he heart not simply functions as a pump but additionally senses the variational strain on itself through the cardiac cycle. Proper mechanical loading is vital for the 915385-81-8 medchemexpress development and maturation on the heart and to keep typical function (Tobita and Keller, 2000). On the other hand, overloading or mechanical stimulus causes cardiac hypertrophy and arrhythmias (Clemo et al., 1998; Sadoshima et al., 1992a; Schrickel et al., 2002). Many 60731-46-6 Description studies have shown that a mechanical stretch or load applied to a cardiac tissue can induce substantial electrophysiological changes by way of the procedure termed “mechano-electric feedback” (MEF). The underlying mechanisms linking such a mechanical influence to subsequent arrhythmias stay unknown. Mechanosensitive channels are proving germane to our understanding of cardiac MEF. The electrophysiological adjustments in the course of MEF have been principally attributed to the activity of stretch-activated ion channels (SACs) (Hu and Sachs, 1997), whose open probability was augmented with increasing membrane tension. Two groups of SACs inside the heart happen to be reported: stretch-activated potassium channels (SAKCs) and stretch-activated non-selective cation channels (SACCs). Current research suggest that the two-pore domain potassium channel TREK-1 may possibly be the molecular entity of SAKCs inside the heart.
