Role of Retinoids x Receptor and Retinoic Acid Receptor in Mouse Liver
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE46762 | GEO | 2013/05/15
SECONDARY ACCESSION(S): PRJNA202289
REPOSITORIES: GEO
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Project description:Genome-wide binding of Retinoids x Receptor in mouse liver was described Using ChIP-Seq data to clarify the role of RXRa in liver
2013-05-15 | E-GEOD-46762 | biostudies-arrayexpress
Project description:The overall study explores differential sensitivity of estrogen-receptor-positive and -negative breast carcinoma cells to retinoids via gene expression and microRNA profiling in MCF7 and MDA-MB-231 cells. This Series reports results of transcriptional profiling of breast carcinoma cell lines comparing the effects of retinoic acid treatment (6 and 48 hours) on estrogen-receptor-positive (MCF7) and estrogen-receptor-negative (MDA-MB-231) cells. mRNA profiling: Retinoic-acid-treated (1microM) vs vehicle-treated cells, two time points (6 and 48h), two cell lines (MCF7 and MDA-MB-231). Two biological replicates for each condition, balanced dye design.
2010-05-21 | E-GEOD-18390 | biostudies-arrayexpress
Project description:The overall study explores differential sensitivity of estrogen-receptor-positive and -negative breast carcinoma cells to retinoids via gene expression and microRNA profiling in MCF7 and MDA-MB-231 cells. This Series reports results of transcriptional profiling of breast carcinoma cell lines comparing the effects of retinoic acid treatment (6 and 48 hours) on estrogen-receptor-positive (MCF7) and estrogen-receptor-negative (MDA-MB-231) cells.
2010-05-21 | GSE18390 | GEO
Project description:Targets of Retinoic Acid (RA) and 3,4-didehydroretinoic acid (ddRA) were identified in primary human epidermal keratinocytes grown in the presence of atRA or ddRA for 4 and 24 hours. Retinoids (natural forms and synthetic derivatives of vitamin A) are used as therapeutic agents for numerous skin diseases such as keratinization disorders (e.g. ichthyoses) and psoriasis. Two endogenous ligands for retinoic acid receptors exist, retinoic acid (atRA) and 3,4-didehydroretinoic acid (ddRA). In primary human epidermal keratinocytes many transcriptional targets for atRA are known, whereas the targets for ddRA are unknown. In an attempt to determine the targets, we compared the effect of atRA and ddRA on transcriptional profiles in undifferentiated and differentiating human primary keratinocytes. First, as expected, many genes were induced or suppressed in response to keratinocyte differentiation. Furthermore, the two retinoids affected substantially more genes in differentiated keratinocytes (more than 350) than in proliferating keratinocytes (20). In differentiating keratinocytes markers of cornification were suppressed suggesting a de-differentiating effect by the two retinoids. When comparing the expression profile of atRA to that of ddRA, no differently regulated genes were found. The array analysis also found that a minor number of miRNAs and a large number of non-coding transcripts were changed during differentiation and in response to the two retinoids. Furthermore, the expression of all, except one, genes known to cause autosomal recessive congenital ichthyosis (ARCI) were found to be induced by differentiation. These results comprehensively document that atRA and ddRA exert similar transcriptional changes in keratinocytes and also add new insights into the molecular mechanism influenced by retinoids in the epidermis. Furthermore, it suggests which ARCI patients could benefit from therapy with retinoids.
2014-08-01 | GSE58749 | GEO
Project description:Targets of Retinoic Acid (RA) and 3,4-didehydroretinoic acid (ddRA) were identified in primary human epidermal keratinocytes grown in the presence of atRA or ddRA for 4 and 24 hours. Retinoids (natural forms and synthetic derivatives of vitamin A) are used as therapeutic agents for numerous skin diseases such as keratinization disorders (e.g. ichthyoses) and psoriasis. Two endogenous ligands for retinoic acid receptors exist, retinoic acid (atRA) and 3,4-didehydroretinoic acid (ddRA). In primary human epidermal keratinocytes many transcriptional targets for atRA are known, whereas the targets for ddRA are unknown. In an attempt to determine the targets, we compared the effect of atRA and ddRA on transcriptional profiles in undifferentiated and differentiating human primary keratinocytes. First, as expected, many genes were induced or suppressed in response to keratinocyte differentiation. Furthermore, the two retinoids affected substantially more genes in differentiated keratinocytes (more than 350) than in proliferating keratinocytes (20). In differentiating keratinocytes markers of cornification were suppressed suggesting a de-differentiating effect by the two retinoids. When comparing the expression profile of atRA to that of ddRA, no differently regulated genes were found. The array analysis also found that a minor number of miRNAs and a large number of non-coding transcripts were changed during differentiation and in response to the two retinoids. Furthermore, the expression of all, except one, genes known to cause autosomal recessive congenital ichthyosis (ARCI) were found to be induced by differentiation. These results comprehensively document that atRA and ddRA exert similar transcriptional changes in keratinocytes and also add new insights into the molecular mechanism influenced by retinoids in the epidermis. Furthermore, it suggests which ARCI patients could benefit from therapy with retinoids. Proliferating and differentiated keratinocytes were harvested after 4 and 24 hours after treatment with atRA, ddRA and vehicle for RNA extraction and hybridization on Affymetrix microarrays. Triplicate samples were generated for each time point and each treatment.
2014-08-01 | E-GEOD-58749 | biostudies-arrayexpress
Project description:About one-third of oestrogen receptor alpha- positive breast cancer patients treated with tamoxifen relapse. Here we identify the nuclear receptor retinoic acid receptor alpha as a marker of tamoxifen resistance. Using quantitative mass spectrometry-based proteomics, we show that retinoic acid receptor alpha protein networks and levels differ in a tamoxifen-sensitive (MCF7) and a tamoxifen-resistant (LCC2) cell line. High intratumoural retinoic acid receptor alpha protein levels also correlate with reduced relapse-free survival in oestrogen receptor alpha-positive breast cancer patients treated with adjuvant tamoxifen solely. A similar retinoic acid receptor alpha expression pattern is seen in a comparable independent patient cohort. An oestrogen receptor alpha and retinoic acid receptor alpha ligand screening reveals that tamoxifen-resistant LCC2 cells have increased sensitivity to retinoic acid receptor alpha ligands and are less sensitive to oestrogen receptor alpha ligands compared with MCF7 cells. Our data indicate that retinoic acid receptor alpha may be a novel therapeutic target and a predictive factor for oestrogen receptor alpha-positive breast cancer patients treated with adjuvant tamoxifen. Peptide and protein identification data set 1: Peptide identification from the MALDI-TOF/TOF data was carried out using the Paragon algorithm in the ProteinPilot 2.0 software package (Applied Biosystems) 46. Default settings for a 4800 instrument were used (i.e., no manual settings for mass tolerance was given). The following parameters were selected in the analysis method: iTRAQ 4plex peptide labelled as sample type, MMTS as alkylating agent of cysteine, trypsin as digesting enzyme, 4800 as instrument, gel based ID and Urea denaturation as special factors, biological modifications as ID focus, and thorough ID as search effort. Peptide identification from the Q-TOF data was carried out using the Spectrum Mill Protein Identification software (Agilent). Data was extracted between MH+ 600 and 4000 Da (Agilent's definition). Scans with the same precursor m/z 90 sec, 0.05 m/z matching with a minimum of 20 peaks in MS2 were merged. Peptide and protein identification data set 2: Proteome discoverer 1.3 with sequest-percolator was used for protein identification. Precursor mass tolerance was set to 10 ppm and for fragments 0.8 Da and 0.02 Da were used for detection in the linear iontrap and the orbitrap, respectively. Oxidized methionine and phosphorylation on S,T and Y was set as dynamic modifications, and carbamidomethylation, N-terminal 8plex iTRAQ, and lysyl 8plex iTRAQ as fixed modifications. Spectra were matched to ensembl 68 limited to human protein sequences, and results were filtered to 1% FDR.
2013-07-24 | PXD000281 | Pride
Project description:Comparison between ChIP-Seq data of RARα and RARβ, between RAR and RXR, as well as between control and retinoic acid-treatment for each investigated nuclear receptors.
2014-01-23 | GSE53736 | GEO
Project description:Comparison between ChIP-Seq data of RAR? and RAR?, between RAR and RXR, as well as between control and retinoic acid-treatment for each investigated nuclear receptors. Mouse were treated by control diet and RA-diet for 1 days. After treatment, livers were used to do ChIP using antibodies of RXR?, RAR?, and RAR?. An aliquote of total chromatin without pull-down process by any antibodies was used as input control. A single-end read of 35bp sequencing was performed on each of ChIPed DNA and input. Sequencing data of RAR? and RAR? were compared to each other. In addtional, each of RAR? and RAR? data were compared with RXR? data. For each nuclear receptor, ChIP-Seq data prior or after RA-treatment were also compared with each other.
2014-01-23 | E-GEOD-53736 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE18390: Effects of retinoids on estrogen-receptor-positive and -negative breast carcinoma cells: mRNA profiling GSE18628: MicroRNA profiling shows different response to retinoids in estrogen-receptor positive and negative cells Refer to individual Series
2010-05-21 | E-GEOD-18693 | biostudies-arrayexpress
Project description:Background & Aims: Alcohol-associated liver disease (ALD) is associated with loss of vitamin A (retinoids), increased steatosis, and greater oxidative stress. Although a strong correlation has been observed between loss of retinoids and ALD, if retinoid loss plays a causal role in the pathophysiology of ALD is not clear. Approach & Results: Based on our prior published data indicating that a selective retinoic acid receptor beta (RARβ) agonist limits nonalcohol-related liver disease (NAFLD) pathology, we generated AlbCre;RARβ knockout (BKO) mice and fed these mice a Lieber DeCarli ethanol diet (ETOH). We also generated cultured human hepatocytes (HepG2) that lack RARβ (RARβ-KO) and treated them with ETOH. Here we show that the livers of BKO mice develop greater steatosis, oxidative stress (assessed by 4-HNE), cell proliferation, and hypertrophy on the ETOH diet when compared to wild type (WT). Compared to ETOH-WT mice, the ETOH-BKO mice also exhibit higher hepatic transcript levels of ATF4, MYC, a subset of integrated stress response (ISR) genes (Trib3, Asns, Nqo1, and Hmox1), and the common ATF4 and MYC target, 4EBP1(EIF4EBP1). In RARβ-KO HepG2 cells, ETOH treatments (24 and 72h) resulted in more rapid and greater development of reactive oxygen species compared to parental HepG2. Notably, even without ETOH, ATF4 protein was higher in the RARβ-KO than in parental HepG2. Conclusions: Our research identifies hepatocyte RARβ as a crucial negative regulator of oxidative stress, MYC, ATF4, and proliferation in ALD.
2023-11-28 | GSE221713 | GEO