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X-ray causes mRNA transcripts change to enhance Orai2-meadated Ca2+ influx in rat brain microvascular endothelial cells

ABSTRACT: X-ray causes mRNA transcripts change to enhance Orai2-meadated Ca2+ influx in rat brain microvascular endothelial cells

PROVIDER: PRJNA699184 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13618850_1.fastq.gz	Fastqsanger.gz
	SRR13618850_2.fastq.gz	Fastqsanger.gz
	SRR13618851_1.fastq.gz	Fastqsanger.gz
	SRR13618851_2.fastq.gz	Fastqsanger.gz
	SRR13618852_1.fastq.gz	Fastqsanger.gz

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X-ray causes mRNA transcripts change to enhance Orai2-meadated Ca2+ influx in rat brain microvascular endothelial cells

Project description:We utilized high-throughput sequencing and subsequent signaling pathway analyses to find all the 2 fold change expression of transcripts in comparison of brain microvascular endothelial cells derived from six Sprague Dawley rats without or with irradiation at the dose of 5 Gy or 20 Gy and then cultured for 12 h or 24 h

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Differentiation and homeostasis of effector Treg cells are regulated by inositol polyphosphates modulating Ca2+ influx

Project description:Activated Foxp3+ regulatory T (Treg) cells differentiate into effector Treg (eTreg) cells to maintain peripheral immune homeostasis and tolerance. T cell receptor (TCR)-mediated induction and regulation of store-operated Ca2+ entry (SOCE) is essential for eTreg cell differentiation and function. However, SOCE regulation in Treg cells remains unclear. Here we show that inositol polyphosphate multikinase (IPMK), which generates inositol tetrakisphosphate and inositol pentakisphosphate, is a pivotal regulator of Treg cell differentiation downstream of TCR signaling. IPMK is highly expressed in TCR-stimulated Treg cells and promotes a TCR-induced Treg cell program. IPMK-deficient Treg cells display aberrant T cell activation and impaired differentiation into RORγt+ Treg cells, and tissue-resident Treg cells. Mechanistically, IPMK controls the generation of higher-order inositol phosphates, thereby promoting Ca2+ mobilization and Treg cell effector functions. Our findings identify IPMK as a critical regulator of TCR-mediated Ca2+ influx and highlight the importance of IPMK in Treg cell-mediated immune homeostasis.

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Fight or flight cardiac responses require augmentation of Ca2+ influx via Rad phosphorylation [RNAseq]

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Circ-CAMTA1 regulated by Ca2+ influx inhibited pyruvate carboxylase activity and modulate T cell function in patients with systemic lupus erythematosus

Project description:The expression profiles of circRNAs in Jurkats cells, co-cultured with and without ionomycin, were analyzed by next-generation sequencing and validated using real-time polymerase chain reaction. The identified Ca2+ influx-regulated circRNAs were further examined in T cells from 42 patients with SLE and 23 healthy controls. The biological function of specific circRNAs was investigated using transfection and RNA pull-down assay. After validation, we confirmed that the expression levels of circ-ERCC4, circ-NFATC2, circ-MYH10, circ-CAMTA1, circ-ASH1L, circ-SOCS7, and circ-ASAP1 were consistently increased in Jurkat cells following Ca2+ influx. The expression levels of circ-CAMTA1, circ-ASH1L, and circ-ASAP1 were significantly lower in T cells from patients with SLE, with even lower levels observed in those with higher disease activity. Interferon (IFN)-α was found to suppress the expression of circ-CAMTA1. Circ-CAMTA1 bound to pyruvate carboxylase and inhibited its biologic activity. Overexpression of circ-CAMTA1, but not its linear form, significantly decreased extracellular glucose levels. Furthermore, increased expression of circ-CAMTA1, but not its linear form, enhanced IL-2 secretion and the protein expression of NFAT1.

2024-11-06 | GSE278650 | GEO

TRPM5 Negatively Regulates Lipopolysaccharide-Induced Ca2+ Signaling of B Lymphocytes

Project description:Ca2+ signaling cascades are essential for various immune cell functions. As such, most cells have negative regulators of Ca2+ homeostasis that strictly regulate cytosolic Ca2+ concentration, such as Ca2+-activated monovalent cation channels (CAMs). Transient receptor potential melastatin-related 5 channel (TRPM5), a CAM, is expressed in B lymphocytes. However, its functional role in the immune system is poorly understood. Here, we show that TRPM5 negatively modulates Ca2+ influx, thereby regulating lipopolysaccharide (LPS)-induced proliferative and inflammatory responses by B cells. Trpm5-deficient mice exhibited increased Ca2+ influx, enhanced proliferative responses, and increased production of inflammatory cytokines interleukin-6 and CXCL10 in LPS-stimulated B cells. However, Ca2+ chelation reduced LPS-induced cytokine production by Trpm5-deficient B cells. Furthermore, Trpm5-deficient mice showed exacerbation of endotoxic shock with high mortality. Our findings demonstrate the importance of TRPM5-dependent regulatory mechanisms in LPS-induced Ca2+ signaling of splenic B cells.

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Differentiation and homeostasis of effector Treg cells are regulated by inositol polyphosphates modulating Ca2+ influx

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ORAI2 promotes BMP9-induced osteogenic differentiation via the MAPK/ERK1/2 and PI3K/AKT pathways in MEFs

Project description:Bone morphogenetic protein (BMP)9 is crucial for osteogenic differentiation. Our RNA-sequencing results revealed that calcium release-activated calcium modulator 2 (ORAI2) was upregulated in mesenchymal stem cells (MSCs) in which osteogenic differentiation was induced by BMP9. ORAI2 is a subunit of store-operated Ca2+ (SOC) channels, which is associated with the second messenger Ca2+. In this study, we found that ORAI2 was downregulated in the bone tissue of ovariectomy (OVX) rats. Subsequently, we examined the impact of ORAI2 on BMP9-induced MSC osteogenic differentiation. Exogenous ORAI2 expression promoted osteogenic differentiation in vitro and bone repair in vivo, whereas silencing ORAI2 inhibited them. Similar results were also revealed using the SOC entry inhibitor SKF96365. Mechanistically, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that the effects of ORAI2 may involve the PI3K/AKT signaling pathway. Consistent with the KEGG analysis results, western blotting results further revealed that exogenous expression of ORAI2 increased the levels of phosphorylated-Akt in cells undergoing BMP9-induced osteogenic differentiation, whereas silencing of ORAI2 reduced them. Furthermore, mass spectrometry results suggested that ORAI2 may bind to IQGAP1, which was confirmed by co-immunoprecipitation and western blotting; notably, ORAI2 could interact with IQGAP1 and then facilitate mitogen-activated protein kinase/ERK1/2 signaling. Our results demonstrated that ORAI2 may promote osteogenic differentiation and play an important role in osteogenesis.

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Rhodococcus qingshengii strain:Ray | isolate:Ray

Project description:Rhodococcus qingshengii strain:Ray | isolate:Ray Genome sequencing

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Differential regulation of membrane potential during store-operated calcium entry in neutrophil subsets

Project description:Calcium signals are initiated in immune cells by the process of store-operated calcium entry (SOCE), where receptor activation triggers transient calcium release from the endoplasmic reticulum, followed by opening of plasma membrane calcium-release activated calcium (CRAC) channels. ORAI1, ORAI2 and ORAI3 are known to comprise the CRAC channel, however the contributions of individual isoforms to neutrophil function is not well understood. Here we show that loss of ORAI1 partially decreases calcium influx while loss of both ORAI1 and ORAI2 completely abolishes store-operated calcium entry. In other immune cell types, loss of ORAI2 enhances SOCE. In contrast, we find that ORAI2-deficient neutrophils display decreased calcium influx, which is correlated with measurable differences in regulation of neutrophil membrane potential via KCa3.1. Decreased SOCE in ORAI1-, ORAI2- and ORAI1/2-deficient neutrophils impairs multiple neutrophil functions including phagocytosis, degranulation, leukotriene and ROS production, rendering ORAI1/2-deficient mice highly susceptible to staphylococcal infection. This study demonstrates that ORAI1 and ORAI2 are the primary components of the neutrophil CRAC channel and identifies novel subpopulations of neutrophils where cell membrane potential functions as a rheostat to modulate the SOCE response. These findings have implications for new mechanisms that modulate neutrophil function during infection, acute and chronic inflammatory conditions, and cancer.

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Annexin A6-mediated tumor suppression requires inhibition of calcium influx and down-regulation of the calcium-activated RasGRF2

Project description:Membrane association of the tumor suppressor, annexin A6 (AnxA6), has been shown to regulate plasma membrane permeability to extracellular Ca2+, inhibit anchorage-independent tumor cell growth and paradoxically, promote tumor cell motility by mechanisms that remains poorly understood. Here, we identified RasGRF2, a Ca2+-activated Ras-specific guanine nucleotide exchange factor, as a major effector of AnxA6-elicited tumor-associated phenotypes in breast cancer cells. We demonstrate that reduced expression or loss of AnxA6 in breast cancer cells is associated with up-regulation of RasGRF2, increased Ras activity and consequently, early onset and rapid growth of xenograft tumors. Meanwhile, up-regulation of AnxA6 in AnxA6-low breast cancer cells is associated with a decrease in Ras activity and growth of xenograft tumors but on the contrary, an increase in Cdc42 activity and EGF-stimulated cell motility. Inhibition of Ca2+ influx into AnxA6-low breast cancer cells via Ni2+-sensitive or non-selective Ca2+ channels dose-dependently suppressed the expression of RasGRF2, induced the expression of AnxA6 and consequently, inhibited tumor cell proliferation. Finally, aberrant expression of RasGRF2 may be triggered by AnxA6-mediated or pharmacological inhibition of non-selective Ca2+ channels and occurs at least in part, by promoter methylation. These data for the first time identify RasGRF2 as a major effector of AnxA6-dependent breast tumor growth and motility and that regulated Ca2+ influx and/or RasGRF2 may be potential therapeutic targets for rapidly growing AnxA6-low breast carcinomas

2015-08-15 | GSE72083 | GEO

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