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Gene expression perturbation upon over-expression of a new PPARG isoform

ABSTRACT: Gene expression perturbation upon over-expression of a new PPARG isoform

PROVIDER: PRJNA493099 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7902416_1.fastq.gz	Fastqsanger.gz
	SRR7902416_2.fastq.gz	Fastqsanger.gz
	SRR7902417_1.fastq.gz	Fastqsanger.gz
	SRR7902417_2.fastq.gz	Fastqsanger.gz
	SRR7902418_1.fastq.gz	Fastqsanger.gz

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Gene expression perturbation upon over-expression of a new PPARG isoform

Project description:PPARγ regulates glucose and lipid homeostasis, insulin signaling and adipocyte differentiation. Here we report the skipping of exon 5 as legitimate splicing event generating PPARγΔ5, a new truncated isoform lacking the ligand binding domain. PPARγΔ5 is endogenously expressed in human adipose tissue and during adipocyte differentiation, lacks the ligand-dependent transactivation ability and acts as dominant negative reducing PPARγ activity. Ligand-mediated PPARγ activation induces exon 5 skipping in a negative feedback loop, suggesting alternative splicing as a new mechanism regulating PPARγ activity. PPARγΔ5 over-expression modifies PPARγ-induced transcriptional network, significantly impairing the differentiation ability of adipocyte precursor cells. Additionally, PPARγΔ5 expression in subcutaneous adipose tissue positively correlates with BMI in two independent cohorts of obese and diabetic patients. From a functional perspective, PPARγΔ5 mimics PPARG dominant negative mutated receptors, possibly contributing to adipose tissue dysfunctions. These findings open unexplored scenario in PPARG regulation and PPARγ-related diseases.

2018-10-14 | GSE120466 | GEO

Gene perturbation after PPARG expression in basal UMUC6 cells

Project description:Gene perturbation after PPARG expression in basal UMUC6 cells

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Isoform-specific functions of PPARg in gene regulation and adipose metabolism

Project description:Peroxisome proliferator-activated receptor g (PPARg) is a nuclear receptor that is a vital regulator of adipogenesis, insulin sensitivity, and lipid metabolism. Activation of PPARg by antidiabetic thiazolidinediones (TZD) reverses insulin resistance but also leads to weight gain that limits the use of these drugs. There are two main PPARg isoforms, but the specific functions of each are not established. Here we generated mouse lines in which endogenous PPARg1 and PPARg2 were epitope-tagged to interrogate isoform-specific genomic binding, and mice deficient in either PPARg1 or PPARg2 to assess isoform-specific gene regulation. Strikingly, although PPARg1 and PPARg2 contain identical DNA binding domains, we uncovered isoform-specific genomic binding sites in addition to shared sites. Moreover, PPARg1 and PPARg2 regulated different set of genes in adipose tissue depots, suggesting distinct roles in adipocyte biology. Indeed, mice with selective deficiency of PPARg1 maintained body temperature better than wild type or PPARg2-deficient mice. Most remarkably, although TZD treatment improved glucose toleranceinsulin resistance in mice lacking either PPARg1 or PPARg2, the PPARg1-deficient mice were protected from TZD-induced body weight gain compared to PPARg2-deficient mice. Thus, PPARg isoforms have specific and separable metabolic functions that may be targeted to improve therapy for insulin resistance and diabetes.

2022-03-25 | GSE186277 | GEO

Gene perturbation after PPARG expression in basal UMUC6 cells

Project description:To better understand the molecular mechanisms underlying PPARG tumor suppressor role in basal cells, we studied the effect of PPARG expression on gene expression levels in UMUC6 cells that express low endogeneous expression levels of PPARG

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Identification of a new PPARG isoform

Project description:PPARγΔ5, a new naturally occurring dominant negative splice isoform impairs PPARγ function and adipocyte differentiation

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C/EBPβ regulates lipid metabolism and Pparg isoform 2 expression in alveolar macrophages

Project description:Pulmonary alveolar proteinosis (PAP) is a syndrome characterized by accumulation of surfactant lipoproteins within the lung alveoli. Alveolar macrophages (AMs) are crucial for surfactant clearance and their differentiation depends on colony-stimulating factor 2 (CSF2) and the establishment of an AM-characteristic gene regulatory network. Here we report that the transcription factor C/EBPβ is essential for the development of the AM identity, as demonstrated by transcriptome and chromatin accessibility analysis. Furthermore, C/EBPβ-deficient AMs showed severe defects in proliferation, phagocytosis and lipid metabolism, collectively resulting in a PAP-like syndrome. Mechanistically, the long C/EBPβ protein variants LAP* and LAP together with CSF2 signaling induced expression of Pparg isoform2, but not isoform1, a molecular regulation that was also observed in other CSF2-primed macrophages. These results uncover C/EBPβ as a key regulator of AM cell fate and as the missing link between CSF2 and Pparg isoform 2 expression, thereby regulating lipid turnover in AMs.

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C/EBPβ regulates lipid metabolism and Pparg isoform 2 expression in alveolar macrophages

Project description:C/EBPβ regulates lipid metabolism and Pparg isoform 2 expression in alveolar macrophages

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Isoform-specific functions of PPARg in gene regulation and adipose metabolism

Project description:Isoform-specific functions of PPARg in gene regulation and adipose metabolism

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Disruption of PPARg signaling results in mouse prostatic intraepithelial neoplasia (mPIN) involving active autophagy

Project description:Peroxisome proliferator-activated receptor-gamma (PPARg) regulates the interface between cellular lipid metabolism, redox status and organelle differentiation. Following conditional prostatic epithelial knockout of PPARg in mice we observed focal hyperplasia of the epithelium which developed to mouse prostatic intraepithelial neoplasia (mPIN), becoming progressively more severe with time. We selectively knocked down PPARg2 isoform in wild-type mouse prostatic epithelial cells and examined the consequences of this in a tissue recombination model. Histopathologically the results resembled the conditional PPARg KO mouse prostates. Electron microscopy showed accumulated defective lysosomes and autophagic vacuoles in both of PPARg- and g2- deficient cells. Gene expression profiling indicated a major dysregulation of cell cycle control and metabolic signaling networks related to peroxisomal and lysosomal maturation, lipid oxidation and degradation. We conclude that PPARg maintains the maturation and turnover of peroxisomes and lysosomes in prostate epithelium. Disruption of PPARg signaling results in autophagy and oxidative stress during mPIN pathogenesis. The mPrE-PPARg knockout and mPrE-PPARg2 shRNA cells were compared to wildtype mPrE cells. Time (3 days culture) and cell types (x 4) were tested.

2010-05-18 | E-GEOD-13867 | biostudies-arrayexpress

PPARg and IL-4-induced gene expression data from PPARg +/- LysCre and PPARg fl/- LysCre mouse bone marrow-derived macrophages

Project description:Conditional macrophage-specific PPARg knockout mice were generated on C57Bl/6 background by breeding PPARg fl/- (one allele is floxed, the other is null) and lysozyme Cre transgenic mice. PPARg and IL-4 signaling was analyzed on bone marrow-derived macrophages. Bone marrow of 3 mice per group was isolated and differentiated to macrophages with M-CSF (20 ng/ml). 20 ng/ml IL-4 was used to induce alternative macrophage activation and 1 uM Rosiglitazone (RSG) was used to activate PPARg. From each mouse 4 samples were generated: 1. M-CSF, 2. M-CSF+RSG, 3. IL-4 and 4. IL-4+RSG. All compounds were added throughout the whole differentiation process, and fresh media was added every other day. Control cells were treated with vehicle (DMSO:ethanol). After 10 days, RNA was isolated and gene expression profiles were analyzed using Mouse Genome 430 2.0 microarrays from Affymetrix. 3 PPARg +/- LysCre and 3 PPARg fl/- LysCre mice were used to isolate bone marrow and from each macrophages were differentiated with or without IL-4 and simultaneously treated with vehicle or RSG. Altogether we analyzed 24 samples with 3 biological replicates as below.

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