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Mus musculus

ABSTRACT: Gene profile of aged Wt, miR-155-/-, miR-146a-/- and DKO CD4+ T cells

PROVIDER: PRJNA252369 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1374080.fastq.gz	Fastqsanger.gz
	SRR1374090.fastq.gz	Fastqsanger.gz
	SRR1374081.fastq.gz	Fastqsanger.gz
	SRR1374091.fastq.gz	Fastqsanger.gz
	SRR1374082.fastq.gz	Fastqsanger.gz

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Gene profile of aged Wt, miR-155-/-, miR-146a-/- and DKO CD4+ T cells

Project description:Differential gene expression profile of CD4+ T cells from 10 months old Wt, miR-155-/-, miR-146a-/- and DKO mice spleens. Wt, miR-155-/-, miR-146a-/- and DKO mice were aged 10 months, CD4+ T cells were sorted from mice spleens for analyses.

2014-12-09 | E-GEOD-58372 | biostudies-arrayexpress

Gene profile of aged Wt, miR-155-/-, miR-146a-/- and DKO CD4+ T cells

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Project description:Gene profile of Wt and miR-155-/- Tfh cells

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Project description:Differential gene expression profile of Tfh and non-Tfh cells from both Wt and miR-155-/- mice spleens. Wt and miR-155-/- mice were immunized with OVA. 8 days post immunization, CD4+CXCR+PD1+ Tfh cells and CD4+CXCR5-PD1- non Tfh cells were sorted from mice spleens for analyses.

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Morphine induced sepsis is mediated by abrogation of endotoxin tolerance through modulation of miR-146a, but not miR-155.

Project description:Endotoxin/LPS tolerance is a tightly regulated phenomenon, which, during infection, prevents systemic hyper-inflammation. Here we report for the first time that morphine reversal of endotoxin tolerance resulting in persistent inflammation thus contributing to septicemia and septic shock. We further report that this regulation is mediated by LPS-induced down-regulation of microRNAs 146a and 155. However, only over-expression of miR-146a, but not miR-155 abrogates morphine mediated hyper-inflammation, while antagonizing miR-146a (but not miR-155) augments morphine mediated hyper-inflammation. Hence, miR-146a could be the potential therapeutic target for morphine-mediated abrogation of endotoxin tolerance.

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Project description:Chronic age-dependent inflammation, or inflammaging, is a risk-factor for many disorders that emerge in aging human populations. Mechanisms underlying these aberrant immune responses are complex and remain to be elucidated. Among recently appreciated regulators of inflammaging are microRNAs; one example of which is the anti-inflammatory miR-146a, where deficient mice succumb to life-shortening chronic inflammation. In this study, we found that deletion of miR-155 in T cells significantly extends the lifespan of miR-146a-/- mice. Using single-cell RNA sequencing and flow cytometry we found that miR-155 promotes the activation of effector T cell populations, including Tfh cells, in mice aged over 15 months. This correlated with miR-155 dependent increases in germinal center B cells, autoantibody responses and serum IgG targeting tissue antigens throughout the body. Mechanistically, we found that the aerobic glycolysis genes are elevated in T cells during aging, and to even greater levels in the absence of miR-146a, and this was reduced upon deleting miR-155 in T cells. Finally, through deletion of the mitochondrial pyruvate carrier (MPC) complex in T cells, which skews metabolism towards aerobic glycolysis, we demonstrate that several of the age-dependent, activation phenotypes of miR-146a-/- T cells were recapitulated, thus revealing the sufficiency of metabolic reprogramming to influence immune cell functions during aging. Altogether, these data indicate that miRNAs play pivotal roles in regulating lifespan through T cell mediated inflammaging.

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