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Effect of Trpc1 or Trpc6 knockout on gene expressions in the hearts of endotoxemic mice

ABSTRACT: Effect of Trpc1 or Trpc6 knockout on gene expressions in the hearts of endotoxemic mice

PROVIDER: PRJNA897808 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22164423_1.fastq.gz	Fastqsanger.gz
	SRR22164423_2.fastq.gz	Fastqsanger.gz
	SRR22164424_1.fastq.gz	Fastqsanger.gz
	SRR22164424_2.fastq.gz	Fastqsanger.gz
	SRR22164425_1.fastq.gz	Fastqsanger.gz

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Effect of Trpc1 or Trpc6 knockout on gene expressions in the hearts of endotoxemic mice

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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Function of the porcine TRPC1 gene in myogenesis and muscle growth

Project description:Muscle growth is a quantitative trait controlled by multiple genes in animals. Previously, we showed that transient receptor potential channel 1 (TRPC1) was a differentially expressed gene in muscle tissues between pig breeds with divergent growth traits using RNA-seq. In this study, we characterized the expression profiles of TRPC1 in different tissues and various pig breeds, and found that TRPC1 is highly expressed in muscle. We found two effective single nucleotide polymorphism (SNP) sites (C-1763T and C-1604T) in TRPC1 that could affect the activity of the promoter region and regulate the growth rate of pigs. Functionally, we used RNAi and overexpression to illustrate that TRPC1 promotes myoblast proliferation, migration, differentiation, fusion, and muscle hypertrophy, while inhibiting muscle degradation, and that these processes may be mediated by activating the Wnt signaling pathways. Taken together, our results revealed that TRPC1 may be a promoter of muscle growth and development and it plays a role in Wnt-mediated myogenesis.

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Analysis of Trpc6 Phosphorylation in HEK293T cells

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2017-08-23 | PXD005482 | Pride

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Project description:Transient receptor potential channel 1 (TRPC1) is a widely expressed mechanosensitive ion channel located within the endoplasmic reticulum membrane, crucial for refilling depleted internal calcium stores during activation of calcium-dependent signaling pathways. Here, we have demonstrated that TRPC1 activity is protective within cartilage homeostasis in the prevention of cellular senescence associated cartilage breakdown during mechanical and inflammatory challenge. We revealed that TRPC1 loss is associated with early stages of osteoarthritis (OA) and plays a non-redundant role in calcium signaling in chondrocytes. Trpc1-/- mice subjected to destabilization of the medial meniscus induced OA developed a more severe OA phenotype than wild type controls. During early OA development, Trpc1-/- mice displayed an increased chondrocyte survival rate, however remaining cells displayed features of senescence including p16INK4a expression and decreased Sox9. RNA sequencing identified differentially expressed genes related to cell number, apoptosis and extracellular matrix organization. Trpc1-/- chondrocytes exhibited accelerated dedifferentiation, while demonstrating an increased susceptibility to cellular senescence. Targeting the mechanism of TRPC1 activation may be a promising therapeutic strategy in osteoarthritis prevention.

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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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