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Transcriptome of cardiac tissue from WT mice, cardiac macrophages depleted mice, and mice deficient for Mertk and LxR

ABSTRACT: Transcriptome of cardiac tissue from WT mice, cardiac macrophages depleted mice, and mice deficient for Mertk and LxR

PROVIDER: PRJNA416139 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6231700.fastq.gz	Fastqsanger.gz
	SRR6231691.fastq.gz	Fastqsanger.gz
	SRR6231701.fastq.gz	Fastqsanger.gz
	SRR6231692.fastq.gz	Fastqsanger.gz
	SRR6231693.fastq.gz	Fastqsanger.gz

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Transcriptome of cardiac tissue from WT mice, cardiac macrophages depleted mice, and mice deficient for Mertk and LxR

Project description:Our study aims to analyze the effect in whole cardiac transcriptome of cardiac macrophage depletion and the lack of receptors implicated in phagocytosis.

2018-10-27 | GSE106295 | GEO

Hepatic transcriptome in wild-type and LXR-deficient mice

Project description:LXR is a transcription factor. Two isoforms exist in mice (alpha and beta). They are both expressed in the liver. We examined the role of LXR by obtaining gene expression profiles from the livers of wild-type and LXR-/- mice from the same genetic background. Liver gene expression was measured from male mice (5 mice/group) of genotypes wild-type and LXR-/- on a mixed Sv129/C57Bl6J background (Repa et al. , 2000, Science, 289(5484):1524-9; Cummins et al., 2006, J Clin Invest,116(7):1902-12) fed for 7 weeks a normal diet (ND) or a Western diet (WD).

2012-11-07 | E-GEOD-38083 | biostudies-arrayexpress

Mertk negatively regulates adaptive immunity

Project description:Tolerogenic dendritic cells (tol-DCs) offer a promising therapeutic potential for autoimmune diseases. Tol-DCs have been reported to inhibit immunogenic responses, yet little is known about the mechanisms controlling their tolerogenic status, as well as associated specific markers. Here we show that the anti-inflammatory TAM receptor tyrosine kinase MERTK, is highly expressed on clinical grade dexamethasone-induced human tol-DCs and mediates their tolerogenic effect. Neutralization of MERTK in allogenic mixed lymphocyte reactions as well as autologous DC-T cell cultures leads to increased T cell proliferation and IFN-g production. Additionally, we identify a previously unrecognized non-cell autonomous regulatory function of MERTK expressed on DCs. Recombinant Mer-Fc protein, used to mimic MERTK on DCs, suppresses naïve and antigen-specific memory T cell activation. This mechanism is mediated by the neutralization of the MERTK agonist Protein S (PROS1) expressed by T cells. We find that MERTK and PROS1 are expressed in human T cells upon TCR activation and drive an autocrine pro-proliferative mechanism. Collectively, these results suggest that MERTK on tol-DCs directly inhibits T cell activation through the competition for PROS1 interaction with MERTK in the T cells. Targeting MERTK may provide an interesting approach to effectively increase or suppress tolerance for the purpose of immunotherapy. The complete database comprised the expression measurements of 54,675 genes for: immature (n=9), mature (n=7) and tolerogenic (n=8). Influence of treatment with dexamethasone (n=3) and LPS (n=2) are included.

2015-01-29 | E-GEOD-56017 | biostudies-arrayexpress

Androgen deprivation in PTEN/LXR -/- mice

Project description:Androgen deprivation in PTEN/LXR -/- mice

| PRJNA554035 | ENA

Hepatic transcriptome in wild-type and LXR-deficient mice

2012-11-07 | GSE38083 | GEO

ATF3 coordinates the survival/proliferation of cardiac macrophages to protect against ischemia-reperfusion injury

Project description:Cardiac resident MerTK+ macrophages exert multiple protective roles post-ischemic injury, however, the mechanisms regulating their fate are not fully understood. Here we show that GAS6-inducible transcription factor ATF3 prevents apoptosis of MerTK+ macrophages after ischemia-reperfusion (IR) injury, by repressing the transcription of multiple genes involved in type I interferon expression (Ifih1 and Infb1) and apoptosis (Apaf1). Mice lacking ATF3 in cardiac macrophages or myeloid cells showed excessive loss of MerTK+ cardiac macrophages, poor angiogenesis, and worse heart dysfunction post-IR, which were rescued by the transfer of MerTK+ cardiac macrophages. GAS6 administration improved cardiac repair in an ATF3-dependent manner. Finally, we showed a negative association of GAS6 and ATF3 expression with the risk of major adverse cardiac events in patients with ischemic heart disease. These results indicate that the GAS6-ATF3 axis has a protective role against IR injury by regulating MerTK+ cardiac macrophage survival/proliferation.

2023-11-07 | GSE247139 | GEO

RNA Sequencing in LXR agonist fed Atp7b-/- mice (Wilson disease)

Project description:The goal of the study was find the gene expression of diverse signaling pathways altered in Atp7b-/- mice (murine WD) liver as compared to control mice and how LXR agonist treatment will improve/ameliorate WD phenotype in Atp7b-/- mice. Activation of LXR/RXR using synthetic LXR agonist ameliorates liver inflammation and fibrosis in murine WD by changing gene expression.

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Effect of LXR agonist T0901317 on the intestinal transcriptome in mice.

Project description:Mice were treated for three days by oral gavage with the synthetic LXR ligand T0901317 (Cayman chemical, USA) using a dose of 50 mg/kg/day in vehicle (0.5% Carboxy-methylcellulose; 400 cPs (Sigma-Aldrich, USA); 0.2% Tween80 (Sigma-Aldrich, USA)) or solely the vehicle (control group). Mice were anesthetized with isoflurane and euthanized by cardiac puncture followed by cervical dislocation. Intestines were flushed with ice cold PBS and frozen in liquid nitrogen.

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2020-07-31 | GSE134137 | GEO

Expression data from macrophages sorted from the heart tissue of WT mice post-IR

Project description:Cardiac resident MerTK+ macrophages exert multiple protective roles post-ischemic injury. To determine the potential reason for the protective role of MerTK+ cardiac macrophages, microarray was performed to identify gene expression profiles on isolated Trem2+, MHCII+, Lyve1+, and MerTK- macrophages from the heart tissue of WT mice post-IR. We investigated the potential reason for the protective role of MerTK+ cardiac macrophages in myocardial Ischemia reperfusion injuryby microarray.

2023-10-31 | GSE246339 | GEO

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