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ScRNA-Seq reveals anti-fibrotic mechanisms of TRPC6 inhibition [scRNA-seq]

ABSTRACT: scRNA-Seq reveals anti-fibrotic mechanisms of TRPC6 inhibition [scRNA-seq]

PROVIDER: PRJNA1120044 | ENA |

REPOSITORIES: ENA

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scRNA-Seq reveals anti-fibrotic mechanisms of TRPC6 inhibition [scRNA-seq]

Project description:Inhibition of transient receptor potential canonical 6 channels (TRPC6) alleviates tubular injury and renal fibrosis induced by unilateral ureteral obstruction (UUO).However, the exact renoprotective mechanisms are unknown. In this study, we utilized single-cell RNA sequencing (scRNA-Seq) to define the cellular and transcriptional landscape associated with renoprotection through in vivo TRPC6 inhibition, specifically using SH045 (larixyl N-methylcarbamate), in the UUO model.

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scRNA-Seq reveals anti-fibrotic mechanisms of TRPC6 inhibition [Spatial Transcriptomics]

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scRNA-Seq reveals anti-fibrotic mechanisms of TRPC6 inhibition [Spatial Transcriptomics]

Project description:scRNA-Seq reveals anti-fibrotic mechanisms of TRPC6 inhibition [Spatial Transcriptomics]

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Identification of pro-fibrotic macrophages populations by scRNA-seq in West Highland white terriers affected with canine idiopathic pulmonary fibrosis

Project description:We used the scRNA-seq to characterize disease-related heterogeneity within cell populations of macrophages/monocytes in the bronchoalveolar lavage fluid from West Highland white terriers either healthy or affected with canine idioapthic pulmonary fibrosis. The disease is still not well understood, occurs in old West Highland white terriers and results from deposition of fibrotic tissue in the lung parenchyma causing respiratory failure.

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Project description:To investigate the mechanism of TRPC1 or TRPC6 on the regulation of endotoxemic cardiac dysfunction, we established Trpc1-/- and Trpc6-/- mice. LPS-challenged endotoxemic mouse model was built, and the gene expression profile was analyzed using data obtained from RNA-seq of WT, LPS-challenged WT, LPS-challenged Trpc1-/-, and LPS-challenged Trpc6-/- mice hearts.

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

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