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CD3254-RXRα Axis Promotes Chemical Reprogramming via RNA Exosome-Mediated MMVL30 Degradation and Inflammation Suppression [RNA-seq]

ABSTRACT: We show that CD-RXRα axis significantly promotes mouse chemical reprogramming of fibroblasts. To identify the molecular mechanisms of CD-RXRα axis in chemical reprogramming, we compared reprogramming efficiency for CD-treated, Rxra-OE and shE3 cells. We then performed RNA-seq for 3 different treatments of 6 samples.

ORGANISM(S): Mus musculus

PROVIDER: GSE208765 | GEO | 2023/05/03

REPOSITORIES: GEO

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CD3254-RXRα Axis Promotes Chemical Reprogramming via RNA Exosome-Mediated MMVL30 Degradation and Inflammation Suppression [CUT&Tag]

Project description:We show that CD-RXRα axis significantly promotes mouse chemical reprogramming of fibroblasts. To identify the molecular mechanisms of CD-RXRα axis in chemical reprogramming, we construct Flag-Rxra-OE cells. We performed Flag-Rxra CUT&Tag with reprogramming intermediate, also we performed CUT&Tag with or without CD treatment for reprogramming intermediates.

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CD3254-RXRα Axis Promotes Chemical Reprogramming via RNA Exosome-Mediated MMVL30 Degradation and Inflammation Suppression

Project description:CD3254-RXRα Axis Promotes Chemical Reprogramming via RNA Exosome-Mediated MMVL30 Degradation and Inflammation Suppression

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CD3254-RXRα Axis Promotes Chemical Reprogramming via RNA Exosome-Mediated MMVL30 Degradation and Inflammation Suppression [RNA-seq]

Project description:CD3254-RXRα Axis Promotes Chemical Reprogramming via RNA Exosome-Mediated MMVL30 Degradation and Inflammation Suppression [RNA-seq]

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CD3254-RXRα Axis Promotes Chemical Reprogramming via RNA Exosome-Mediated MMVL30 Degradation and Inflammation Suppression [CUT&Tag]

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Epithelial RXRα activity induced by Westernization of diet instigates enteritis in Crohn’s disease

Project description:Westernization of diet, partly characterised by excess of long-chain fatty acids, provides a risk for developing Crohn’s disease (CD), and perturbs the function of specialized intestinal epithelium termed Paneth cells. The lack of a cellular and molecular framework of lipid sensing in intestinal inflammation poses a constraint to understanding detrimental effects of Western diets. Here, we report how Paneth cell sensing of lipid excess in a Western diet is translated into CD-like intestinal inflammation. Small intestinal transcriptional profiling of CD patients from three independent cohorts identified increased activity of the transcription factor retinoid x receptor alpha (RXRα) specifically in intestinal epithelium. Intestinal epithelial RXRα activity was induced by polyunsaturated fatty acid (PUFA) excess in a Western diet in mice with CD-like enteritis. PUFA-induced RXRα activity in Paneth cells governed chronic transmural enteritis by enabling the expression of the interleukin 8 homologue CXCL1. Blockade of PUFA-induced RXRα activity by 9-cis retinoic acid ameliorated CXCL1 production and enteritis, and patients receiving isotretinoin therapy (a precursor for 9-cis retinoic acid) displayed reduced odds of developing CD. Collectively, we identify Paneth cells as gatekeepers of lipid stress that exploit RXRα to sense and translate PUFA excess into enteritis, which could be targeted to prevent or treat CD.

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RXRα Modulates Hepatic Stellate Cell Activation and Liver Fibrosis by Targeting CaMKKβ-AMPKα Axis

Project description:Hepatic stellate cells (HSCs) represent a dominant fibrogenic cell population in the liver, whose activation is a key event in the development and progression of hepatic fibrosis. We report here that retinoid X receptor-alpha (RXRα), a unique member of the nuclear receptor superfamily, is a critical modulator of HSC activation and liver fibrosis through its regulation of calcium/calmodulin-dependent protein kinase kinase β (CaMKKβ)-mediated activation of AMP-activated protein kinase-alpha (AMPKα). K-80003, which binds RXRα by a unique mechanism, effectively inhibits the activation, proliferation and migration of HSCs and inhibits liver fibrosis in the CCl4 and AMLN animal models by AMPKα activation, which promotes mitophagy in HSCs. Mechanistically, K-80003 activation of AMPKα requires its induction of RXRα formation of condensates with CaMKKβ and AMPKα via a two-phase mechanism. The formation of RXRα condensates is mediated by the N-terminal intrinsically disorder region of RXRα and is dependent on its phosphorylation by CaMKKβ. Our results therefore unravel an important RXRα-CaMKKβ-AMPKα axis in the modulation of HSC activation through phase separation and identify K-80003 as a potent inhibitor of HSC activation and liver fibrosis by targeting the axis.

2025-09-14 | GSE277363 | GEO

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Project description:Insulin action initiates a series of phosphorylation events regulating cellular differentiation, growth and metabolism. We have previously discovered, in a mass spectrometry-based phosphoproteomic study, that insulin/IGF-1 signaling induces phosphorylation of retinoid x receptor alpha (RXRα) at S22 in mouse brown pre-adipocytes. Here, we show that insulin induces the phosphorylation of RXRα at S22 in both brown precursor and mature adipocytes through a pathway involving ERK, downstream of IRS-1 and -2. We also found that RXRα S22 phosphorylation is promoted by insulin and upon re-feeding in brown adipose tissue in vivo, and that insulin-stimulated S22 phosphorylation of RXRα is dampened by diet-induced obesity. We used Rxra knockout cells re-expressing wild type (WT) or S22A non-phosphorylatable forms of RXRα to further characterize the role of S22 in brown adipocytes. Knockout of Rxra in brown pre-adipocytes resulted in decreased lipid accumulation and adipogenic gene expression during differentiation, and re-expression of RxraWT alleviated these effects. However, we observed no significant difference in cells re-expressing the RxraS22A mutant as compared with the cells re-expressing RxraWT. Furthermore, comparison of gene expression during adipogenesis in the WT and S22A re-expressing cells by RNA sequencing revealed similar transcriptomic profiles. Thus, our data propose a dispensable role for RXRα S22 phosphorylation in adipogenesis and transcription in differentiating brown pre-adipocytes.

2020-03-30 | GSE147687 | GEO

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