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

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

PROVIDER: PRJNA555419 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9700090.fastq.gz	Fastqsanger.gz
	SRR9700091.fastq.gz	Fastqsanger.gz
	SRR9700082.fastq.gz	Fastqsanger.gz
	SRR9700092.fastq.gz	Fastqsanger.gz
	SRR9700083.fastq.gz	Fastqsanger.gz

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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.

2020-06-01 | GSE134443 | GEO

TRAF5 negatively regulates TLR signaling in B lymphocytes.

Project description:The cytoplasmic adaptor proteins TNFR-associated factor (TRAF)3 and TRAF6 are important mediators of TLR signaling. To our knowledge, we show in this study for the first time that another TRAF family member, TRAF5, is a negative regulator of TLR signaling. B lymphocytes from TRAF5(-/-) mice produced more IL-6, IL-12p40, IL-10, TNF-?, and IgM than did wild-type B cells after TLR stimulation. Consistent with these data, exogenous overexpression of TRAF5 in B cells inhibited TLR-mediated cytokine and Ab production. TLR stimulation of TRAF5-deficient B cells did not affect cell survival, proliferation, or NF-?B activation but resulted in markedly enhanced phosphorylation of the MAPKs ERK1/2 and JNK. TRAF5 negatively regulated TLR signaling in a cell-specific manner, because TRAF5(-/-) macrophages and dendritic cells showed less dramatic differences in TLR-mediated cytokine production than B cells. Following TLR stimulation, TRAF5 associated in a complex with the TLR adaptor protein MyD88 and the B cell-specific positive regulator of TLR signaling TAB2. Furthermore, TRAF5 negatively regulated the association of TAB2 with its signaling partner TRAF6 after TLR ligation in B cells. To our knowledge, these data provide the first evidence that TRAF5 acts as a negative regulator of TLR signaling.

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Low incubation temperature during early development negatively affects survival and related innate immune processes in zebrafish larvae exposed to lipopolysaccharide

Project description:Low incubation temperature during early development negatively affects survival and related innate immune processes in zebrafish larvae exposed to lipopolysaccharide

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Tet2 negatively regulates memory fidelity

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BLIMP1 negatively regulates IL-2 signaling in T cells

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BLIMP1 negatively regulates IL-2 signaling in T cells

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BLIMP1 negatively regulates IL-2 signaling in T cells

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Astrocyte Ca2+ Influx Negatively Regulates Neuronal Activity.

Project description:Maintenance of neural circuit activity requires appropriate regulation of excitatory and inhibitory synaptic transmission. Recently, glia have emerged as key partners in the modulation of neuronal excitability; however, the mechanisms by which glia regulate neuronal signaling are still being elucidated. Here, we describe an analysis of how Ca2+ signals within Drosophila astrocyte-like glia regulate excitability in the nervous system. We find that Drosophila astrocytes exhibit robust Ca2+ oscillatory activity manifested by fast, recurrent microdomain Ca2+ fluctuations within processes that infiltrate the synaptic neuropil. Unlike the enhanced neuronal activity and behavioral seizures that were previously observed during manipulations that trigger Ca2+ influx into Drosophila cortex glia, we find that acute induction of astrocyte Ca2+ influx leads to a rapid onset of behavioral paralysis and a suppression of neuronal activity. We observe that Ca2+ influx triggers rapid endocytosis of the GABA transporter (GAT) from astrocyte plasma membranes, suggesting that increased synaptic GABA levels contribute to the neuronal silencing and paralysis. We identify Rab11 as a novel regulator of GAT trafficking that is required for this form of activity regulation. Suppression of Rab11 function strongly offsets the reduction of neuronal activity caused by acute astrocyte Ca2+ influx, likely by inhibiting GAT endocytosis. Our data provide new insights into astrocyte Ca2+ signaling and indicate that distinct glial subtypes in the Drosophila brain can mediate opposing effects on neuronal excitability.

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