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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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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.

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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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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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