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Inhibiting L-type calcium channel promotes cardiomyocyte proliferation through activating canonical Wnt signaling pathway

ABSTRACT: Inhibiting L-type calcium channel promotes cardiomyocyte proliferation through activating canonical Wnt signaling pathway

PROVIDER: PRJNA769587 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16248351_1.fastq.gz	Fastqsanger.gz
	SRR16248351_2.fastq.gz	Fastqsanger.gz
	SRR16248352_1.fastq.gz	Fastqsanger.gz
	SRR16248352_2.fastq.gz	Fastqsanger.gz
	SRR16248353_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Inhibiting L-type calcium channel promotes cardiomyocyte proliferation through activating canonical Wnt signaling pathway

Project description:We performed RNA-Seq analysis of neoatal rat ventricular cardiomyocytes (NRVCs) and human pluripotent stem cells derived cardiomyocytes (hPSC-CMs) which were treated with Nimodipine (NM) to investigate the moleclular mechanism of inhibiting L-type calcium channel (LTCC) to promote cardiomyocyte proliferation.

2022-10-10 | GSE185542 | GEO

DEGs resulting from activating L-type calcium channel, CaV1.2, in mouse valvular interstitial cells (mVICs).

Project description:We report differentially expressed genes as a result of activation of L-type calcium channel CaV1.2 with GOF mutation in mVICs.

2021-06-01 | GSE151520 | GEO

DEGs resulting from activating L-type calcium channel, CaV1.2, in mouse valvular interstitial cells (mVICs).

Project description:DEGs resulting from activating L-type calcium channel, CaV1.2, in mouse valvular interstitial cells (mVICs).

| PRJNA636195 | ENA

The β2-subunit of voltage-gated calcium channels inhibits cardiomyocyte hypertrophy through a channel-independent mechanism.

Project description:L-type voltage-gated calcium channels (LTCCs) regulate crucial physiological processes in the heart. They are composed of the Cav1 pore-forming subunit and the accessory subunits Cav, Cav2 and Cav. Cav is a cytosolic soluble protein that regulates channel trafficking and activity, but it also exerts other LTCC-independent functions. Cardiac hypertrophy, a relevant risk factor for the development of congestive heart failure, depends on the activation of calcium-dependent pro-hypertrophic signaling cascades; however, the role of LTCCs in this pathology remains controversial. Here, by using shRNA-mediated Cav silencing, we demonstrate that Cav2 downregulation enhances 1-adrenergic receptor agonist-induced cardiomyocyte hypertrophy in an LTCC-independent manner. We report that a pool of Cav2 is targeted to the nucleus in cardiomyocytes and that the expression of this nuclear fraction decreases during in vitro and in vivo induction of cardiac hypertrophy. Moreover, the overexpression of nucleus-targeted Cav2 in cardiomyocytes inhibits in vitro-induced hypertrophy. Quantitative proteomic analyses showed that Cav2 knockdown leads to changes in the expression of diverse myocyte proteins, including reduction of calpastatin, an endogenous inhibitor of the calcium-dependent protease calpain. Accordingly, Cav2-deficient cardiomyocytes had a two-fold increase in calpain activity as compared to control cells. Furthermore, inhibition of calpain activity in Cav2-deficient cells abolished the enhanced 1-adrenergic receptor agonist-induced hypertrophy observed in these cells. Our findings indicate that in cardiomyocytes, a nuclear pool of Cav2 participates in cellular functions that are independent of LTCC activity. They also indicate that a downregulation of nuclear Cav2 during cardiac hypertrophy promotes the activation of calpain-dependent hypertrophic pathways.

2021-09-09 | PXD016483 | Pride

The mutant Moonwalker TRPC3 channel links calcium signaling to lipid metabolism in the developing

Project description:The Moonwalker (Mwk) mouse is a model of dominantly inherited cerebellar ataxia caused by a gain-of-function mutation in the transient receptor potential (TRP) channel TRPC3. We report impairments in dendritic growth and synapse formation early on during Purkinje cell development in the Mwk cerebellum that are accompanied by alterations in calcium signaling.

2015-06-01 | E-MTAB-3517 | biostudies-arrayexpress

Sustained L-type Calcium Channel Blockade Alters Gene Regulation in the Adult Mouse Ventricle

Project description:Objective: L-type calcium channels (LTCC) homeostatically regulate calcium on a beat by beat basis, but also provide Ca that over long time scales may contribute to transcriptional regulation. We previously showed that sustained LTCC blockade (CCB) elicits LTCC remodeling in ventricular cardiac myocytes (CM). Here we hypothesize that sustained CCB has broad effects on the expression of genes involved in calcium handling. Methods and Results: Therefore, we subjected adult mice to sustained CCB for 24 hours and performed gene expression profiling. In comparison to vehicle-only control animals, 231 genes were up-regulated, and 111 genes were down-regulated by sustained LTCC blockade (p <0.01). Gene ontology analysis suggested that the CaMKIIdelta signaling pathway was up-regulated in these cells. Unexpectedly, phosphorylation of phospholamban (PLN) at threonine17 (Thr17), an index of CaMKIIdelta activity, was not changed by sustained CCB; however, the degree of phosphorylation of the neighboring PLN-Ser16 substrate site for PKA was significantly reduced by sustained CCB compared to control. Gene expression profiling suggested no change in PKA, but it showed that protein phosphatase 2A (PP2A) mRNA increased, and immunoblots demonstrated that PP2Ac-alpha protein was significantly increased by sustained CCB. Consistent with elevated PP2Ac-alpha protein expression LTCC exhibited decreased phosphorylation of the C-terminal Ser1928 PKA substrate site. Conclusions: We conclude that sustained CCB elicits a spectrum of transcriptional events, including compensatory up-regulation of LTCC and PP2Ac-alpha. Although this study is restricted to mouse, these results suggest the new hypothesis that clinically-relevant sustained LTCC blockade in humans results in changes in gene regulation in the heart. Keywords: L-type calcium channel, calcium channel blockade, verapamil

2009-12-31 | GSE8367 | GEO

Transcriptome profiling of liver derived from calcium channel ITPR2 KO mice

Project description:Transcriptome profiling of liver derived from calcium channel ITPR2 KO mice

| PRJNA587751 | ENA

Calcium channel β3 subunit regulates ATP-dependent migration of dendritic cells

Project description:Calcium channel β3 subunit regulates ATP-dependent migration of dendritic cells

| PRJNA933110 | ENA

Impact of the Voltage-Gated Calcium Channel Antagonist Nimodipinedipine on the Development of Oligodendrocyte Precursor Cells

Project description:We investigated the effects of nimodipine, a L-type voltage-gated calcium channel antagonist, on the expression profile of myelin genes in the oligodendrocyte precursor cell (OPC) line Oli-Neu. We performed gene expression profiling analysis using data obtained from RNA-seq of four biological replicates for treatment and four replicates for control condition.

2023-03-30 | GSE221939 | GEO

Cardiac-specific deletion of voltage dependent anion channel 2 leads to dilated cardiomyopathy by altering calcium homeostasis

Project description:Voltage dependent anion channel 2 (VDAC2) is an outer mitochondrial membrane porin known to play a significant role in apoptosis and calcium signaling. Abnormalities in calcium homeostasis often leads to electrical and contractile dysfunction and can cause dilated cardiomyopathy and heart failure. However, the specific role of VDAC2 in intracellular calcium dynamics and cardiac function is not well understood. To elucidate the role of VDAC2 in calcium homeostasis, we generated a cardiac ventricular myocyte-specific developmental deletion of Vdac2 in mice. Our results indicate that loss of VDAC2 in the myocardium causes severe impairment in excitation-contraction coupling by altering both intracellular and mitochondrial calcium signaling. We also observed adverse cardiac remodeling which progressed to severe cardiomyopathy and death. Reintroduction of VDAC2 in 6-week-old knock-out mice partially rescued the cardiomyopathy phenotype. Activation of VDAC2 by efsevin increased cardiac contractile force in a mouse model of pressure-overload induced heart failure. In conclusion, our findings demonstrate that VDAC2 plays a crucial role in cardiac function by influencing cellular calcium signaling. Through this novel role in cellular calcium dynamics and excitation-contraction coupling VDAC2 emerges as a plausible therapeutic target for heart failure.

2021-03-09 | GSE168487 | GEO

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