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Transcriptome profiling of liver derived from calcium channel ITPR2 KO mice

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

PROVIDER: PRJNA587751 | ENA |

REPOSITORIES: ENA

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Transcriptome profiling of liver derived from calcium channel ITPR2 KO mice

Project description:Cellular senescence is induced by multiple stresses and results in a stable proliferation arrest accompanied by a pro-inflammatory secretome. Senescent cells accumulate during aging, promoting various age-related pathologies and thus limiting lifespan. The endoplasmic reticulum ITPR2 release channel and calcium fluxes from the ER to the mitochondria have been identified as drivers of cellular senescence in human cells. Here we show that Itpr2 knockout mice display improved aging such as increased lifespan, a better response to metabolic stress, less immunosenescence, as well as less liver steatosis and fibrosis. Cellular senescence, which is known to promote these alterations, is decreased in both Itpr2 KO mice and Itpr2 KO embryo-derived cells. Interestingly, ablation of ITPR2 in vivo and in vitro decreases the number of contacts between the mitochondria and the ER and forced contacts between these two organelles induce premature senescence in normal cells. These new findings shed light on the role of contacts and facilitated exchanges between the ER and the mitochondria through ITPR2 in regulating senescence and physiological aging.

2019-11-06 | GSE139967 | GEO

Transcriptome profiling of early or late passage MEFs derived from calcium channel ITPR2 KO mice

2019-11-06 | GSE139982 | GEO

Transcriptome profiling of early or late passage MEFs derived from calcium channel ITPR2 KO mice

Project description:Transcriptome profiling of early or late passage MEFs derived from calcium channel ITPR2 KO mice

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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

Lack of TRPV1 Channel Modulates Mouse Gene Expression and Liver Proteome with Glucose Metabolism Changes

Project description:To investigate the role of the transient receptor potential channel vanilloid type 1 (TRPV1) channel in hepatic glucose metabolism, we performed proteomics analysis of the liver of C57Bl/6J (WT) and Trpv1 KO mice (n = 4 per group). Liver from Trpv1 KO mice showed significant proteomics changes consistent with enhanced glycogenolysis, as well as increased gluconeogenesis and inflammatory features.

2022-06-21 | MSV000089696 | MassIVE

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

Identifying the Transcriptome Signature of Calcium Channel Blocker in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes

Project description:Identifying the Transcriptome Signature of Calcium Channel Blocker in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes

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The calcium-permeable channel OSCA1.3 regulates plant stomatal immunity

Project description:Perception of biotic and abiotic stresses often leads to stomatal closure in plants. Rapid influx of calcium ions (Ca2+) across the plasma membrane plays an important role in this response, but the identity of Ca2+ channels involved has remained elusive. Here, we report that the Arabidopsis thaliana Ca2+-permeable channel OSCA1.3 controls stomatal closure during immunity. OSCA1.3 is rapidly phosphorylated upon perception of pathogen-associated molecular patterns (PAMPs). Biochemical and quantitative phospho-proteomics analyses reveal that the immune receptor associated cytosolic kinase BIK1 interacts with and phosphorylates the N-terminal cytosolic loop of OSCA1.3 within minutes of treatment with the peptidic PAMP flg22 derived from bacterial flagellin.

2020-09-11 | PXD020852 | panorama

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

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