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Ventricles of wild type and TRPC6 knockout hearts

ABSTRACT: To determine the effect of genetic deletion of TRPC6 in the cardiomyocytes, we compared the mRNA expression levels in the ventricle of a wild-type mouse and a TRPC6 genetic deletion mouse.

ORGANISM(S): Mus musculus

PROVIDER: GSE288700 | GEO | 2026/02/04

REPOSITORIES: GEO

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Ventricles of wild type and TRPC6 knockout hearts

Project description:Ventricles of wild type and TRPC6 knockout hearts

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Myocardial TRPC6-mediated Zn2+ influx induces beneficial positive inotropy through b-adrenoceptors

Project description:Baroreflex control of cardiac contraction (positive inotropy) through sympathetic nerve activation is important to maintain cardiocirculatory homeostasis. Transient receptor potential canonical subfamily (TRPC) channels are responsible for alfa1-adrenoceptor (alfa1AR)-stimulated cation entry and their upregulation is reportedly associated with pathological cardiac remodeling, but whether TRPC channels participate in physiological pump functions remains unclear. Here, we demonstrate that TRPC6-specific Zn2+ influx potentiates alfa-adrenoceptor (alfaAR)-stimulated positive inotropy in rodent cardiomyocytes. Deletion of the trpc6 gene impairs sympathetic nerve-activated positive inotropy, but not chronotropy in mice. TRPC6-mediated Zn2+ influx boosts alfa1AR-stimulatedalfaAR/Gs-dependent signaling in rat cardiomyocytes by inhibiting alfa-arrestin-mediated alfaAR internalization. Replacing two TRPC6-specific amino acids in the pore region with those of TRPC3 diminishes the alfa1AR-stimulated Zn2+ influx and positive inotropic response. Pharmacological enhancement of TRPC6-mediated Zn2+ influx prevents the progression of heart failure in dilated cardiomyopathy mice. Our data provide evidence that TRPC6-mediated Zn2+ influx with α1AR stimulation enhances baroreflex-induced positive inotropy, which may be a new therapeutic strategy for chronic heart failure.

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Analysis of Trpc6 Phosphorylation in HEK293T cells

Project description:The aim of this project was to detect phosphorylation on the human calcium Channel TRPC6. TRPC6 is mutated in genetic diseases of the podocyte, a postmitotic cell at the epithelial filtration barrier

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Inducing ferroptosis to impede metastasis by inhibiting the calcium channel TRPC6

Project description:TRPC6 (transient receptor potential cation channel 6) contributes to the ability of breast cancer cells to persist after chemotherapy. Here, we investigated a potential function of TRPC6 in enabling breast cancer cells to resist stimuli that induce ferroptosis. A minority population of quiescent cells was isolated from triple-negative breast cancer (TNBC) cell lines using a p27 reporter. These p27+ cells exhibited increased TRPC6 expression and resistance to ferroptosis compared to the p27- proliferating population. The p27+ cells were also more metastatic than the p27- cells supporting the hypothesis that metastasis requires the ability of cells to evade ferroptosis. In pursuit of the mechanism involved, we discovered that the ability of TRPC6 to repress c-Myc is essential because repression of c-Myc sustains levels of glutathione that are sufficient to impede ferroptosis. Importantly, treatment of TNBC cells with a TRPC6 inhibitor reduced metastasis significantly, an effect that was mitigated by liproxstatin-1 treatment. These results support the hypothesis that a sub-population of TNBC cells characterized by TRPC6 expression has the potential to form metastases by evading ferroptosis.

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Expression study between dental pulp cells from TRPC6-mut individual and control individuals

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Project description:Arterial pulmonary hypertension is a rare disease, with little knowledge regarding its etiology, and high mortality. Development of right and later on also left ventricular heart insufficiency, secondary to pulmonary hypertension, is a negative predictive factor. Genetic and molecular processes underlying left heart ventricle remodeling over the course of pulmonary hypertension remain unknown. In particular, there is no knowledge regarding the mechanisms of left heart ventricle atrophy which was completely avoided by researchers until recently.The aim of this study was to assess changes in protein abundance in left and right heart ventricle free wall of rats in monocrotaline model of PAH.

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