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PPARγ controls alveolar macrophage identity [part1]

ABSTRACT: Tissue-resident macrophages comprise heterogeneous populations with unique functions and distinct gene expression signatures. While it has been established that they mostly originate from embryonic progenitors, the signals inducing a characteristic tissue-specific differentiation program remain unknown. Here we identify PPARγ as the crucial transcription factor determining perinatal alveolar macrophage (AM) development and identity. Development of the fetal monocyte derived AM precursor was largely abrogated in CD11c-Cre/Ppargfl/fl mice. To reveal the underlying changes in gene expression, we performed microarray analysis of sorted WT and KO AM and pre-AM from 3 different timepoints. Part1: d2 and d11 sorts & array

ORGANISM(S): Mus musculus

PROVIDER: GSE60247 | GEO | 2014/09/28

SECONDARY ACCESSION(S): PRJNA257838

REPOSITORIES: GEO

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PPARÎ³ controls alveolar macrophage identity [part1]

Project description:Tissue-resident macrophages comprise heterogeneous populations with unique functions and distinct gene expression signatures. While it has been established that they mostly originate from embryonic progenitors, the signals inducing a characteristic tissue-specific differentiation program remain unknown. Here we identify PPARÎ³ as the crucial transcription factor determining perinatal alveolar macrophage (AM) development and identity. Development of the fetal monocyte derived AM precursor was largely abrogated in CD11c-Cre/Ppargfl/fl mice. To reveal the underlying changes in gene expression, we performed microarray analysis of sorted WT and KO AM and pre-AM from 3 different timepoints. Part1: d2 and d11 sorts & array pre-AM FACS-sorted from lungs of d2 and mature AM from d11 PPARgfl/fl (WT) and CD11c-cre/PPARgfl/fl (KO) mice and subsequently processed for RNA extraction and hybridization on Affymetrix microarrays. 2 biological replicates per group, each composed of pooled cells from 2 individual mice

2014-09-28 | E-GEOD-60247 | biostudies-arrayexpress

PPARγ controls alveolar macrophage identity [part2]

Project description:Tissue-resident macrophages comprise heterogeneous populations with unique functions and distinct gene expression signatures. While it has been established that they mostly originate from embryonic progenitors, the signals inducing a characteristic tissue-specific differentiation program remain unknown. Here we identify PPARγ as the crucial transcription factor determining perinatal alveolar macrophage (AM) development and identity. Development of the fetal monocyte derived AM precursor was largely abrogated in CD11c-Cre/Ppargfl/fl mice. To reveal the underlying changes in gene expression, we performed microarray analysis of sorted WT and KO AM and pre-AM from 3 different timepoints. Part2: adult sorts & array

2014-09-28 | GSE60248 | GEO

PPARÎ³ controls alveolar macrophage identity [part2]

Project description:Tissue-resident macrophages comprise heterogeneous populations with unique functions and distinct gene expression signatures. While it has been established that they mostly originate from embryonic progenitors, the signals inducing a characteristic tissue-specific differentiation program remain unknown. Here we identify PPARÎ³ as the crucial transcription factor determining perinatal alveolar macrophage (AM) development and identity. Development of the fetal monocyte derived AM precursor was largely abrogated in CD11c-Cre/Ppargfl/fl mice. To reveal the underlying changes in gene expression, we performed microarray analysis of sorted WT and KO AM and pre-AM from 3 different timepoints. Part2: adult sorts & array AM FACS-sorted from lungs of adult PPARgfl/fl (WT) and CD11c-cre/PPARgfl/fl (KO) mice and subsequently processed for RNA extraction and hybridization on Affymetrix microarrays. 2 biological replicates per group, each composed of pooled cells from 2 individual mice

2014-09-28 | E-GEOD-60248 | biostudies-arrayexpress

The effect of lncRNA PART1 knockdown on gene expression in HCC1806 and HCC1395 cells

Project description:PART1 was knocked down down using GapmeRs specific to PART1. The breast cancer cells used in this study were confirmed to have PART1 expression by qPCR and knockdown of PART was confirmed by qPCR.

2021-02-28 | GSE156114 | GEO

RNA sequencing of PART1 knockdown by siRNA in ovarian cancer cells

Project description:The expression of lncRNA PART1 was found to be significantly upregulated in platinum-sensitive patients with ovarian cancer, and this upregulation was positively correlated with a favorable prognosis. Cellular experiments demonstrated that inhibition of PART1 led to cellular senescence and increased resistance to cisplatin and PARP inhibitors. Thus, LncRNA PART1 is a novel target for overcoming resistance to PARP inhibitors in ovarian cancer.

2024-02-01 | GSE253450 | GEO

The effect of lncRNA PART1 knockdown on mature miRNA levels in HCC1806 and HCC1395 cells

2021-02-28 | GSE163569 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of lncRNA PART1 Regulated Transcriptomes

Project description:The goals of this study are to analyze the transcriptome profiling (RNA-seq) after lncRNA PART1 overexpression in MGC-803 cells.

2022-09-09 | GSE137074 | GEO

PPARγ lipodystrophy mutants reveal intermolecular interactions required for enhancer activation

Project description:The peroxisome proliferator-activated receptor γ (PPARγ) is the master regulator of adipocyte differentiation, and mutations that interfere with PPARγ function cause lipodystrophy. Structural studies indicate that PPARγ domains engage in several intra- and inter-moleuclar interactions; however, how these interactions modulate the ability of PPARγ to activate target genes in a cellular context is currently poorly understood. Here we analysed the transcriptional potential of R212Q and E379K two previously uncharacterised lipodystrophy-associated PPARγ mutants that are located in distinct PPARγ domains but are both predicted to affect intermolecular interactions. Using a combination of biochemical and genome-wide approaches we show that these mutations impair binding to an overlapping subset of enhancers that are less accessible and specifically require PPARγ for chromatin remodeling. Based on these findings we propose a model in which recruitment of PPARγ to chromatin is determined by several intermolecular interfaces. Furthermore, our data exemplify that relatively subtle molecular defects in transcription factors are sufficient to significantly affect enhancer binding and thereby transcriptional output.

2022-09-08 | PXD036589 | Pride

Mus musculus

Project description:PPARγ controls alveolar macrophage identity [part1]

| PRJNA257838 | ENA

Histone H3K9 Methyltransferase G9a Represses PPARγ Expression and Adipogenesis [Affymetrix expression data]

Project description:PPARγ promotes adipogenesis while Wnt proteins inhibit adipogenesis. However, the mechanisms that control expression of these positive and negative master regulators of adipogenesis remain incompletely understood. By genome-wide histone methylation profiling in preadipocytes, we find that among gene loci encoding adipogenesis regulators, histone methyltransferase (HMT) G9a-mediated repressive epigenetic mark H3K9me2 is enriched on the entire PPARγ locus. H3K9me2 and G9a levels decrease during adipogenesis, which correlates inversely with induction of PPARγ. Removal of H3K9me2 by G9a deletion enhances chromatin opening and binding of adipogenic transcription factor C/EBP-beta to PPARγ promoter, which promotes PPARγ expression. Interestingly, G9a represses PPARγ expression in an HMT activity-dependent manner but facilitates Wnt10a expression independent of its enzymatic activity. Consistently, deletion of G9a or inhibiting G9a HMT activity promotes adipogenesis. Finally, deletion of G9a in mouse adipose tissues increases adipogenic gene expression and tissue weight. Thus, by inhibiting PPARγ expression and facilitating Wnt10a expression, G9a represses adipogenesis. Examination of gene expression changes in G9a KO brown preadipocytes

2013-02-01 | E-GEOD-41456 | biostudies-arrayexpress

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