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The effects of CD4 T cell Nr4a family on NASH progression

ABSTRACT: The effects of CD4 T cell Nr4a family on NASH progression

PROVIDER: PRJNA1008561 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25739765_1.fastq.gz	Fastqsanger.gz
	SRR25739765_2.fastq.gz	Fastqsanger.gz
	SRR25739766_1.fastq.gz	Fastqsanger.gz
	SRR25739766_2.fastq.gz	Fastqsanger.gz
	SRR25739767_1.fastq.gz	Fastqsanger.gz

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The effects of CD4 T cell Nr4a family on NASH progression

Project description:NASH is characterized by hepatic steatosis, inflammation, fibrosis and liver damage, which eventually results in liver dysfunction due to cirrhosis or hepatocellular carcinoma. However, the cellular and molecular mechanisms underlying NASH progression remain largely unknown. In this study, we aimed to elucidate the impact of Nr4a family in CD4 T cells in NASH development.

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The effects of CD4 T cell Nr4a family on NASH progression (RNA-Seq)

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The effects of CD4 T cell Nr4a family on NASH progression (RNA-Seq)

Project description:The effects of CD4 T cell Nr4a family on NASH progression (RNA-Seq)

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Elucidation of roles of Nr4a nuclear orphan receptors and Foxp3 in thymic Treg cell development

Project description:Both Nr4a family nuclear orphan receptors and Foxp3 had been revealed to be crucial transcription factors in Treg cell development. In this study, to reveal their roles in a Treg cell developmental transcriptional programs, we compared transcriptomes among wild-type conventional CD4 T (Tconv) cells, wild-type Treg cells, Nr4a-triple-knockout (Nr4a-TKO) Treg precursor (preTreg) cells, and Foxp3-KO preTreg cells by microarray.

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NASH

Project description:Non-alcoholic fatty liver disease (NAFLD) is characterized by a series of pathological changes that can progress from simple fatty liver disease to non-alcoholic steatohepatitis (NASH). The objective of this study is to describe changes in global gene expression associated with the progression of NAFLD. This study is focused on the expression levels of genes responsible for the absorption, distribution, metabolism and excretion (ADME) of drugs. Differential gene expression between three clinically defined pathological groups; normal, steatosis and NASH was analyzed. The samples were diagnosed as normal, steatotic, NASH with fatty liver (NASH fatty) and NASH without fatty liver (NASH NF). Genome-wide mRNA levels in samples of human liver tissue were assayed with Affymetrix GeneChipM-. Human 1.0ST arrays

2011-07-12 | E-MEXP-3291 | biostudies-arrayexpress

Gene expression profiles of wild type and Nr4a-triple knockout (Nr4a-TKO) Tnaive and iTreg 3 h

Project description:In this study, we investigated the roles of Nr4a family transcription factors in Th and Treg cell differentiation from Tnaive cells. Nr4a factors were found to promote Treg cell differentiation and repress Th1 and Th2 differentiation. During Treg cell differentiation, all Nr4a factors are transiently induced in Tnaive cells immediately after TCR stimulation, whereby they mediate epigenetic changes directly or by cooperating with other transcription factors. To reveal Nr4a factors' mediated transcrptional events, we analyzed gene expression of wild type and Nr4a-tripple knockout (Nr4a-TKO) Tnaive and iTreg cells by microarray analysis.

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Gene expression profiles of wild type, Nr4a-triple knockout (Nr4a-TKO), and Foxp3-KO iTreg 24 h

Project description:In this study, we investigated the roles of Nr4a family transcription factors in Th and Treg cell differentiation from Tnaive cells. Nr4a factors were found to promote Treg cell differentiation and repress Th1 and Th2 differentiation. During Treg cell differentiation, all Nr4a factors are transiently induced in Tnaive cells immediately after TCR stimulation, whereby they mediate epigenetic changes directly or by cooperating with other transcription factors. To reveal Nr4a factors' mediated transcrptional events, we analyzed gene expression of wild type and Nr4a1,a2,a3-tripple knockout (Nr4a-TKO) iTreg cells by microarray analysis.

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Project description:The diverse T cell receptor (TCR) repertoire – generated randomly through VDJ recombination early in development – is inherently self-reactive. Clonal deletion and diversion to regulatory T cell (Treg) fate are key central tolerance mechanisms engaged during thymic selection. The NR4A family of transcription factors has been implicated in both, but the extent of its contribution to clonal deletion and the transcriptional mechanisms at play remain unknown. Here, we investigated both NR4A-dependent and NR4A-independent transcriptional changes induced in developing thymocytes in response to model self-antigen presented by medullary thymic epithelial cells (mTECs). To do so, we took advantage of the MHCII-restricted TCR transgene OTII and model self-antigen (membrane-bound ovalbumin expressed under the control of the rat insulin promoter encoded by the RIP-mOVA transgene). Our results suggest that a surprisingly broad transcriptional program is enacted upon high affinity self-antigen encounter in the thymus. Furthermore, by investigating the expression profile of OTII Nr4a1-/- Nr4a3-/- double knock-out (OTII-DKO) thymocytes that receive high affinity antigen-dependent signal but escape both clonal deletion and Treg diversion, we reveal evidence for deletional and non-deletional central tolerance mechanisms.

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Project description:Nonalcoholic fatty liver disease (NAFLD) ranges from steatosis to nonalcoholic steatohepatitis (NASH), that often progresses to hepatocellular carcinoma (HCC) through a largely undefined mechanism. NASH and HCC both depend on inflammatory signaling whose master regulator is the NFκB transcription factor family, activated by canonical and non-canonical pathways. Here, we investigated non-canonical NFκB-inducing kinase (NIK/MAP3K14) in metabolic NASH, NASH to HCC transition as well as in DEN-induced HCC. We revealed that hepatocyte-specific NIK deficiency (NIKLKO) ameliorated metabolic NASH complications and reduced hepatocarcinogenesis however, independent of its role in NFB pathway. Instead, hepatic NIK attenuated hepatoprotective JAK2/STAT5 signaling that is a prerequisite for NASH and NASH to HCC progression in mice and humans. Our data suggest NIK-mediated inhibitory JAK2 phosphorylation at serine 633 that might be amenable for future therapeutic interventions in patients.

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Tid1 Deficiency Disrupting Mitochondria to Drive NASH-Dependent Hepatocellular Carcinoma Progression

Project description:Non-alcoholic fatty liver disease/steatohepatitis (NAFLD/NASH) is a significant risk factor for hepatocellular carcinoma (HCC). However, a preclinical model of progressive NAFLD/NASH is largely lacking. Here, we report that mice with hepatocyte-specific deletion of Tid1, encoding a mitochondrial cochaperone, tended to develop NASH-dependent HCC. Mice with hepatic Tid1 deficiency showed impairing mitochondrial function and causing fatty acid metabolic dysregulation; meanwhile, sequentially developed fatty liver, NASH, and cirrhosis/HCC in a diethylnitrosamine (DEN) induced oxidative environment. The pathological signatures of human NASH, including cholesterol accumulation and activation of inflammatory and apoptotic signaling pathways, are also present in these mice. Clinically, low Tid1 expression was associated with unfavorable prognosis in patients with HCC. Empirically, hepatic Tid1 deficiency directly disrupts entire mitochondria that play a key role in the NASH-dependent HCC development. Overall, we established a new mouse model that develops NASH-dependent HCC and provides a promising approach to improve the treatment.

2022-06-02 | E-MTAB-9973 | biostudies-arrayexpress

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