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LRH-1 Mitigates Intestinal Inflammatory Disease by Maintaining Epithelial Homeostasis and Cell Survival

ABSTRACT: LRH-1 Mitigates Intestinal Inflammatory Disease by Maintaining Epithelial Homeostasis and Cell Survival

PROVIDER: PRJNA479409 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7466770.fastq.gz	Fastqsanger.gz
	SRR7466771.fastq.gz	Fastqsanger.gz
	SRR7466772.fastq.gz	Fastqsanger.gz
	SRR7466773.fastq.gz	Fastqsanger.gz
	SRR7466774.fastq.gz	Fastqsanger.gz

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LRH-1 Mitigates Intestinal Inflammatory Disease by Maintaining Epithelial Homeostasis and Cell Survival

Project description:We report the gene expression changes in murine small intestinal organoids following deletion of LRH-1 (NR5A2) and humanization by expression of human LRH-1 in mouse LRH-1 knockout organoids.

2018-07-04 | GSE116563 | GEO

LRH-1 mitigates intestinal inflammatory disease by maintaining epithelial homeostasis and cell survival.

Project description:Epithelial dysfunction and crypt destruction are defining features of inflammatory bowel disease (IBD). However, current IBD therapies targeting epithelial dysfunction are lacking. The nuclear receptor LRH-1 (NR5A2) is expressed in intestinal epithelium and thought to contribute to epithelial renewal. Here we show that LRH-1 maintains intestinal epithelial health and protects against inflammatory damage. Knocking out LRH-1 in murine intestinal organoids reduces Notch signaling, increases crypt cell death, distorts the cellular composition of the epithelium, and weakens the epithelial barrier. Human LRH-1 (hLRH-1) rescues epithelial integrity and when overexpressed, mitigates inflammatory damage in murine and human intestinal organoids, including those derived from IBD patients. Finally, hLRH-1 greatly reduces disease severity in T-cell-mediated murine colitis. Together with the failure of a ligand-incompetent hLRH-1 mutant to protect against TNFα-damage, these findings provide compelling evidence that hLRH-1 mediates epithelial homeostasis and is an attractive target for intestinal disease.

| S-EPMC6180039 | biostudies-literature

Transcriptional analysis of adult LRH-1 knockout livers reveals a novel role for LRH-1 in hepatic lipid homeostasis and phospholipid remodeling

Project description:Purpose: To identify novel LRH-1 target genes in adult knockout livers.

2020-01-01 | GSE109431 | GEO

Vascular integrity is essential for maintaining tissue homeostasis

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Vascular integrity is essential for maintaining tissue homeostasis

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TAK1-dependent checkpoint in dendritic cell survival regulates immune homeostasis and function

Project description:Homeostatic control of dendritic cell (DC) survival is crucial for a productive adaptive immune response, but the molecular mechanism is not well defined. Moreover, how DCs influence homeostasis of the immune system under steady state remains unclear. Combining DC-specific and inducible deletion systems, we report here that the kinase TAK1 is an essential regulator of DC survival and immune system homeostasis and function. Deficiency of TAK1 in CD11c+ cells diminished DC populations, especially the CD8+ and CD103+ DC subsets in the lymphoid and non-lymphoid organs, respectively. This was associated with increased apoptosis of DCs, whereas DC proliferation and differentiation from precursors appeared largely normal. In addition, acute deletion of TAK1 caused DC apoptosis, indicating a direct role of TAK1 in actively maintaining DC survival. TAK1 deficiency impaired activities of the pro-survival NF-kB and AKT pathways but upregulated expression of the pro-apoptotic molecule Bim. Under steady state, loss of TAK1 in DCs resulted in a myeloid proliferative disorder, and altered homeostasis of T cells. In response to antigen stimulation, TAK1-deficient DCs were impaired for T cell priming and regulatory T cell generation. Therefore, TAK1 orchestrates a pro-survival checkpoint in DCs that affects the homeostasis and function of the immune system RNA extracted from three replicate samples of wild-type and Map3k7 (TAK1) knockout dendritic cells was analyzed on Affymetrix gene expression arrays

2012-01-23 | E-GEOD-34417 | biostudies-arrayexpress

Global hepatic transcript data from LRH-1 hep+/+ and LRH-1 hep-/- livers

Project description:Transcript data from LRH-1 hep+/+ and LRH-1 hep-/- livers from mice fed ad libitum and sacrificed at 7 am We used microarrays to detail the global programme of gene expression underlying hepatic function in ad libitum fed mice.

2014-07-11 | GSE59305 | GEO

Global hepatic transcript data from LRH-1 WT and LRH-1 K289R livers

Project description:Transcript data from LRH-1 WT and LRH-1 K289R livers from mice fed ad libitum and sacrificed at 7 am We used microarrays to detail the global programme of gene expression underlying hepatic function in ad libitum fed mice.

2014-07-11 | GSE59304 | GEO

Global hepatic transcript data from LRH-1 WT and LRH-1 K289R jejunums

Project description:Transcript data from LRH-1 WT and LRH-1 K289R jejunums from mice fed ad libitum and sacrificed at 7 am We used microarrays to detail the global programme of gene expression underlying jejunal function in ad libitum fed mice.

2014-07-11 | GSE59303 | GEO

LRH-1 governs vital transcriptional programs in endocrine sensitive and resistant breast cancer cells: LRH-1 ChIP-seq

Project description:Tumor characteristics are decisive in the determination of treatment strategy for breast cancer patients. Patients with estrogen receptor a(ERa)-positive breast cancer can benefit from long-term hormonal treatment. Nonetheless, the majority of patients will develop resistance to these therapies. Here, we investigated the role of the nuclear receptor liver receptor homolog-1 (LRH-1, NR5A2) in anti-estrogen (AE) sensitive and resistant breast cancer cells. We identified genome-wide LRH-1 binding sites using ChIP-seq, uncovering preferential binding to regions distal to transcriptional start sites (TSS). We further characterized these LRH-1 binding sites by integrating overlapping layers of specific chromatin marks, revealing that many LRH-1 binding sites are active and could be involved in long-range enhancer-promoter looping. Combined with transcriptome analysis of LRH-1 depleted cells, these results show that LRH-1 regulates specific subsets of genes involved in cell proliferation in AE-sensitive and AE-resistant breast cancer cells. Furthermore, the LRH-1 transcriptional program is highly associated with a signature of poor outcome and high-grade breast cancer tumors in vivo. Herein we report the genome-wide location and molecular function of LRH-1 in breast cancer cells and reveal its therapeutic potential for the treatment of breast cancers, notably for tumors resistant to treatments currently used in therapies.

2014-02-27 | GSE47027 | GEO

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