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Prdm16 overexpression effect on inguinal white adipose tissue:stromal-vascular cells

ABSTRACT: Prdm16 overexpression effect on inguinal white adipose tissue:stromal-vascular cells

PROVIDER: PRJNA530011 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8818372.fastq.gz	Fastqsanger.gz
	SRR8818373.fastq.gz	Fastqsanger.gz
	SRR8818374.fastq.gz	Fastqsanger.gz
	SRR8818375.fastq.gz	Fastqsanger.gz
	SRR8818376.fastq.gz	Fastqsanger.gz

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Prdm16 overexpression effect on inguinal white adipose tissue:stromal-vascular cells

Project description:Analysis of SV cells transducted with control or Prdm16 retrovirus. Results provide insight into molecular mechanism underlying Prdm16 function in iWAT white adipose tissues.

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Gene expression of adipocyte and stromal-vascular fractions

Project description:In order to select mRNA transcripts strongly enriched in murine white adipocytes versus brown adipocytes or stromal-vascular fraction, gene expression data of the adipocyte and stromal-vascular fractions of the interscapular brown, inguinal subcutaneous as well as visceral epididymal adipose tissue depots of young adult male C57BL/6 mice housed at constant 23Â°C ambient temperature were obtained. 18 samples: 3 different adipose tissues separated into stromal-vascular fraction and adipocytes, analyzed in biological triplicates.

2013-04-27 | E-GEOD-44059 | biostudies-arrayexpress

Gene expression of adipocyte and stromal-vascular fractions

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PPARg agonists induce a white-to-brown fat conversion through stabilization of PRDM16 protein

Project description:Brown adipose tissue dissipates energy through heat and functions as a defense against cold and obesity. PPARγ ligands have been shown to induce the browning of white adipocytes; however, the underlying mechanisms remain unclear. Here we show that PPARγ ligands require full agonism to induce a brown fat gene program preferentially in subcutaneous white adipose. These effects require expression of PRDM16, a factor that controls the development of classical brown fat. Depletion of PRDM16 blunts the effects of the PPARγ agonist rosiglitazone on the induced brown fat gene program. Conversely, PRDM16 and rosiglitazone synergistically activate the brown fat gene program in vivo. This synergy is tightly associated with an increased accumulation of PRDM16 protein, due in large measure to an increase in the half-life of the protein in agonist treated cells. Identifying compounds that stabilize PRDM16 protein may represent a novel therapeutic pathway for the treatment of obesity and diabetes. Microarray analysis of the differentiated inguinal adipocytes expressing sh-scr or sh-PRDM16 in the presence or absence of rosiglitazone (1uM). These samples were profiled using Affymetrix mouse 430A_2 arrays, representing 2 biological replicates for each samples (8 samples in total).

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Exercise Training Remodels Inguinal White Adipose Tissue Through Adaptations in Innervation, Vascularization and the Extracellular Matrix

Project description:Inguinal white adipose tissue (iWAT) is essential for the beneficial effects of exercise training on metabolic health. The underlying mechanisms for these effects are not fully understood and here, we test the hypothesis that exercise training results in a more favorable iWAT structural phenotype. Using biochemical, imaging, and multi-omics analyses we find that 11-days of wheel running in male mice causes profound iWAT remodeling including decreased extracellular matrix (ECM) deposition, increased vascularization and innervation. We identify adipose stem cells as one of the main contributors to training-induced ECM remodeling, show that the PRDM16 transcriptional complex is necessary for iWAT remodeling and beiging, and discover neuronal growth regulator 1 (NEGR1) as a link between PRDM16 and neuritogenesis. Moreover, we find that training causes a shift from hypertrophic to insulin-sensitive adipocyte subpopulations. Exercise training leads to remarkable adaptations to iWAT structure and cell-type composition that can confer beneficial changes in tissue metabolism.

2023-10-24 | PXD040894 | Pride

miRNA expression in inguinal adipose tissues

Project description:We asked if miRNAs are involved in PRDM16 protein expression. Thus microarray was employed with inguinal adipose tissues from contol, fasted and cold exposure C57BL/6J male mice In this dataset, we include all the miRNA expression data obtained from dissected mouse inguinal adipose tissues from control, fasted and cold exposure mice. Generally, microRNAs (miRNAs) are small non-coding RNAs that negatively regulate gene expression at the post-transcriptional level. Based on previous results, we asked whether miRNAs are involved in the regulation of PRDM16 in ingWAT in response to different physiological stimuli. We therefore performed miRNA microarray analysis using ingWAT from the cold-exposed mice, the fasted mice and the control mice. Given that cold exposure increased the level of PRDM16 protein whereas fasting decreased its expression, miRNAs that have expression patterns opposite to that of PRDM16 were selectedã??

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Project description:Committed preadipocyte fibroblasts were genetically labelled in transgenic mice by expressing GFP under the control of the locus for Zfp423, a gene controlling preadipocyte determination. These mice are herein referred to as Zfp423-GFP mice. The overall goal was to identify genes differentially expressed between adipogenic GFP+ firboblasts and non-adipogenic GFP- fibroblasts from either inguinal or epididymal fat stromal vascular cultures obtained from Zfp423-GFP mice. Adipose stromal vascular cultures were obtained from inguinal or epididymal fat of 6-8 week-old male Zfp423-GFP mice. GFP+ and GFP- fibroblasts were sorted from fat stromal vascular cultures and then returned to culture. Subconfluent cultures of GFP+ and GFP- cells were compared in triplicate for Affymetrix analysis.

2011-12-31 | E-GEOD-34775 | biostudies-arrayexpress

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Project description:To assess the influences of a crude medicinal herb extract (MHE) on the immune composition and function in inguinal white adipose tissue (iWAT), we isolated iWAT stromal vascular fractions (SVFs) from control (PBS) and MHE-treated mice and performed RNA-seq analysis. iWAT SVF of mice treated with MHE was defined as the treatment group. Phosphate-buffered saline (PBS) treatment was used as the control group. Then RNA-Seq experiment was performed by OE Biotech Co., Ltd. (Shanghai, China) to analyze gene expression changes in iWAT SVF.

2024-10-09 | GSE279130 | GEO

Asc-1 regulates white versus beige adipocyte fate in a subcutaneous stromal cell population

Project description:Here we provide scRNAseq data from the stromal vascular fraction of adult (8 weeks) and adolescent (2 weeks) murine inguinal subcutaneous white adipose tissue. This allows studying cellular composition and cellular heterogeneity within subcutaneous fat.

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PRDM16 Deficiency in Vascular Smooth Muscle Cells Aggravates Abdominal Aortic Aneurysm

Project description:Abdominal aortic aneurysm (AAA) is usually asymptomatic until life-threatening complications occur, predominantly involving aortic rupture. Currently, no drug-based treatments are available, primarily due to limited understanding of AAA pathogenesis. The transcriptional regulator PR domain–containing protein 16 (PRDM16) is highly expressed in the aorta, but its functions in the aorta are largely unknown. By RNA-seq analysis, we found that vascular smooth muscle cell–specific (VSMC-specific) Prdm16-knockout (Prdm16SMKO) mice already showed extensive changes in the expression of genes associated with extracellular matrix (ECM) remodeling and inflammation in the abdominal aorta under normal housing conditions without any pathological stimuli. Human AAA lesions displayed lower PRDM16 expression. Periadventitial elastase application to the suprarenal region of the abdominal aorta aggravated AAA formation in Prdm16SMKO mice. During AAA development, VSMCs undergo apoptosis because of both intrinsic and environmental changes, including inflammation and ECM remodeling. Prdm16 deficiency promoted inflammation and apoptosis in VSMCs. A disintegrin and metalloproteinase 12 (ADAM12) is a gelatinase that can degrade various ECMs. We found that ADAM12 is a target of transcriptional repression by PRDM16. Adam12 knockdown reversed VSMC apoptosis induced by Prdm16 deficiency. Our study demonstrated that PRDM16 deficiency in VSMCs promoted ADAM12 expression and aggravates AAA formation, which may provide potential targets for AAA treatment.

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