Identification of the Regulatory Roles of LncPLAAT3-AS in Porcine Adipocyte Differentiation and Lipogenesis
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ABSTRACT:
PROVIDER: PRJNA883198 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the role of lncPLAAT3-AS in adipocyte differentiation, we overexpressed and inhibited lncPLAAT3-AS in primary adipocytes from pigs. We then performed gene expression profiling using data obtained from RNA-seq of a total of three different cells in two different treatments and a blank control.
2023-02-06 | GSE213924 | GEO
Project description:The Mediator complex functions as a control center orchestrating diverse signalings, gene activities, and biological processes. However, how Mediator subunits determine distinct cell fates remains to be fully elucidated. Here, we show that Mediator MED23 controls the cell fate preference that directs differentiation into smooth muscle cells (SMCs) or adipocytes. Med23-deficiency facilitates SMC differentiation but represses adipocyte differentiation from the multipotent mesenchymal stem cells. Gene profiling revealed that the presence or absence of Med23 oppositely regulates two sets of genes: the RhoA/MAL-targeted cytoskeleton/SMC genes and the Ras/ELK1 targeted growth/adipocyte genes. Mechanistically, MED23 favors ELK1-SRF binding to SMC gene promoters for repression, whereas the lack of MED23 favors MAL-SRF binding to SMC gene promoters for activation. Remarkably, the effect of MED23 on SMC differentiation can be recapitulated in zebrafish embryogenesis. Collectively, our data demonstrate the dual, opposing roles for MED23 in regulating the cytoskeleton/SMC and growth/adipocyte gene programs, suggesting its “Ying-Yang” function in directing adipogenesis vs. SMC differentiation. Examination of SRF enrichment in sictrl and si23 10T1/2 cells
2012-12-20 | E-GEOD-40369 | biostudies-arrayexpress
Project description:G-protein-coupled receptors (GPCRs) are membrane proteins that enable cells to sense molecular signals and to respond in a broad range of biological processes according to the circumstances of cells. Recent studies elucidated that short-medium chain fatty acids can stimulate GPCRs to activate signaling pathways for adipocyte differentiation. As for differentiation of Porcine Subcutaneous Pre-Adipocyte (PSPA), it has been demonstrated that octanoate supplementation in differentiation medium is essential for growth arrest which triggers differentiation initiation of PSPA followed by lipid synthesis and accumulation to develop into fully matured adipocyte. Previously we detected 10 candidate GPCR genes considered to affect adipocyte differentiation of PSPA. Transfection of small interfering RNA (siRNA) for the candidate genes indicated that knockdown of three genes (A, B and C) obviously decreased the differentiation of PSPA. Therefore we investigated gene expression profiles of PSPA transfected with siRNA for each of three GPCR genes using a porcine custom microarray. Our result indicated that larger numbers of down-regulated genes were detected more than up-regulated genes by the siRNA transfection. Gene ontology analysis elucidated that genes up-regulated by knockdown of Gene A, B and C were categorized in biological processes of skeletal system development, mitosis, and cell adhesion, respectively. Interestingly, knockdown of all three genes commonly down-regulated genes categorized in PPAR signaling pathway and immune response. Differentiation of PSPA might be attributable to the alteration of gene expression profiles regulated by GPCRs identified in this study.
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Project description:In this study, we explored the roles of microRNAs in adipocyte differentiation and metabolism. We first knocked down Argonaute2 (Ago2), a key enzyme in the processing of micro-RNAs (miRNAs), to investigate a potential role for miRNAs in adipocyte differentiation and/or metabolism. Although we did not observe dramatic differences in adipogenesis between Ago2 knock-down and control 3T3-L1 cells, incorporation of [(14)C]glucose or acetate into triacylglycerol, and steady-state levels of triacyglycerol were all reduced, suggesting a role for miRNAs in adipocyte metabolism. To study roles of specific miRNAs in adipocyte biology, we screened for miRNAs that are differentially expressed between preadipocytes and adipocytes for the 3T3-L1 and ST2 cell lines. Distinct subsets of miRNAs decline or increase during adipocyte conversion, whereas most miRNAs are not regulated. One locus encoding two miRNAs, 378/378*, contained within the intron of PGC-1beta is highly induced during adipogenesis. When overexpressed in ST2 mesenchymal precursor cells, miRNA378/378* increases the size of lipid droplets and incorporation of [(14)C]acetate into triacylglycerol. Although protein and mRNA expression levels of C/EBPalpha, C/EBPbeta, C/EBPdelta, and PPARgamma1 are unchanged, microarray and quantitative RT-PCR analyses indicate that a set of lipogenic genes are upregulated, perhaps due to increased expression of PPARgamma2. Knock-down of miRNA378 and/or miRNA378* decreases accumulation of triacylglycerol. Interestingly, we made the unexpected finding that miRNA378/378* specifically increases transcriptional activity of C/EBPalpha and C/EBPbeta on adipocyte gene promoters.
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Project description:The Mediator complex functions as a control center orchestrating diverse signalings, gene activities, and biological processes. However, how Mediator subunits determine distinct cell fates remains to be fully elucidated. Here, we show that Mediator MED23 controls the cell fate preference that directs differentiation into smooth muscle cells (SMCs) or adipocytes. Med23-deficiency facilitates SMC differentiation but represses adipocyte differentiation from the multipotent mesenchymal stem cells. Gene profiling revealed that the presence or absence of Med23 oppositely regulates two sets of genes: the RhoA/MAL-targeted cytoskeleton/SMC genes and the Ras/ELK1 targeted growth/adipocyte genes. Mechanistically, MED23 favors ELK1-SRF binding to SMC gene promoters for repression, whereas the lack of MED23 favors MAL-SRF binding to SMC gene promoters for activation. Remarkably, the effect of MED23 on SMC differentiation can be recapitulated in zebrafish embryogenesis. Collectively, our data demonstrate the dual, opposing roles for MED23 in regulating the cytoskeleton/SMC and growth/adipocyte gene programs, suggesting its “Ying-Yang” function in directing adipogenesis vs. SMC differentiation.
2012-12-20 | GSE40369 | GEO
Project description:We attempted to analyze the effect of adipocyte-specific knockout of Prmt1 in energy homeostasis in mice. By analyzing the transcriptomics of epididymal primary adipocytes from male mice with wild type and adipocyte-specific Prmt1 knockout mice, we provide the insight into the collective roles of Prmt1 in epididymal white adipose tissues.
2021-02-25 | GSE167446 | GEO
Project description:These data show time-course transcriptional profiling of porcine subcutaneous preadipocyte cell line (PSPA) during differentiation. In the early stage after stimulation for adipocyte differentiation, upregulation of many genes encoding proteins involved in regulation of cell proliferation and transcription was observed. The data presented here should form a valuable database for exploring candidate genes for fat-related QTLs in pigs, and also for analyses to clarify the physiological characteristics of development of porcine adipose tissues by comparison with the results in humans and mice.
2011-11-27 | GSE26907 | GEO
Project description:We attempted to analyze the effect of adipocyte-specific knockout of Crtc2 in in aging. By analyzing the transcriptomics of epididymal primary adipocytes from male mice with wild type and adipocyte-specific Crtc2 knockout mice in response to aging, we provide the insight into the collective roles of Crtc2 in epididymal white adipose tissues upon aging.
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Project description:Dysfunctional adipose tissue is believed to promote the development of hepatic steatosis and systemic insulin resistance, but many of the mechanisms involved are still unclear. Lipin 1 catalyzes the conversion of phosphatidic acid to diacylglycerol (DAG), the penultimate step of triglyceride synthesis, which is essential for lipid storage. Herein we found that adipose tissue LPIN1 expression is decreased in people with obesity compared to lean subjects and low LPIN1 expression correlated with multi-tissue insulin resistance and increased rates of hepatic de novo lipogenesis. Comprehensive metabolic and multi-omic phenotyping demonstrated that adipocyte-specific Lpin1-/- mice had a metabolically-unhealthy phenotype, including liver and skeletal muscle insulin resistance, hepatic steatosis, increased hepatic de novo lipogenesis, and transcriptomic signatures of nonalcoholic steatohepatitis that was exacerbated by high-fat diets. We conclude that adipocyte lipin 1-mediated lipid storage is vital for preserving adipose tissue and systemic metabolic health and its loss predisposes mice to nonalcoholic steatohepatitis.
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