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Robust single nucleus RNA sequencing reveals depot-specific cell population dynamics in adipose tissue remodeling during obesity

ABSTRACT: Robust single nucleus RNA sequencing reveals depot-specific cell population dynamics in adipose tissue remodeling during obesity

PROVIDER: PRJNA1086907 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28305146_1.fastq.gz	Fastqsanger.gz
	SRR28305146_2.fastq.gz	Fastqsanger.gz
	SRR28305147_1.fastq.gz	Fastqsanger.gz
	SRR28305147_2.fastq.gz	Fastqsanger.gz
	SRR28305148_1.fastq.gz	Fastqsanger.gz

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Robust single nucleus RNA sequencing reveals depot-specific cell population dynamics in adipose tissue remodeling during obesity

Project description:Single nucleus RNA sequencing (snRNA-seq), an alternative to single cell RNA sequencing (scRNA-seq), encounters technical challenges in obtaining high-quality nuclei and RNA, persistently hindering its applications. Here, we present a robust technique for isolating nuclei across various tissue types, remarkably enhancing snRNA-seq data quality. Employing this approach, we comprehensively characterize the depot-dependent cellular dynamics of various cell types underlying adipose tissue remodeling during obesity. By integrating nuclear RNA-seq data from adipocyte nuclei of varying sizes, we identify distinct adipocyte subpopulations categorized by size and functionality. Specifically, we characterize dysfunctional hypertrophic adipocytes prevalent in visceral adipose tissues during obesity, exhibiting cellular stress, inflammation and impaired metabolic gene expression. Obesity-induced changes in gene expression profiles of adipocyte subpopulations reveal their distinct contributions to adipose tissue pathophysiology. Our study establishes a robust snRNA-seq method, providing novel insights into the mechanisms orchestrating adipose tissue remodeling during obesity, with broader applicability across diverse biological systems.

2024-04-01 | GSE261417 | GEO

Robust snRNA-seq protocol revealing mouse white adipose tissue remodeling during obesity

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Obesity drives depot-specific vascular remodeling in white adipose tissue

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Obesity drives depot-specific vascular remodeling in white adipose tissue

Project description:Obesity-driven pathological expansion of white adipose tissue (WAT) is a key driver of endothelial dysfunction. Contrary to this paradigm, early vascular alterations associated with over nutrition also exacerbate AT dysfunction. To dissect this complex cause and consequence relationship, here we perform a single-cell transcriptomics screen to generate a detailed landscape of endothelial heterogeneity and vascular alterations in murine model of obesity. Given the differences in ontogeny and function of distinct WAT depots, we demarcate key differences in subcutaneous and visceral WAT vasculature. In addition to descriptive taxonomy, we perform in-depth validation and characterization of our in silico data. We identify a sWAT specific fenestrated endothelial cell subtype, which is drastically reduced in obese conditions. This reduction was associated with a decrease in VEGFA expressing perivascular cells. The novel endothelial subtypes provide a basis for future research and new directions for therapeutic interventions.

2023-05-26 | E-MTAB-12855 | biostudies-arrayexpress

Robust snRNA-seq protocol revealing mouse white adipose tissue remodeling during obesity

Project description:Robust snRNA-seq protocol revealing mouse white adipose tissue remodeling during obesity

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Elevated Extra-cellular Matrix Signaling in Adipose Mesothelial Cells is Linked to Insulin Resistance in Obesity

Project description:Visceral adipose tissue fibrosis is linked to metabolic dysfunction in obesity; however, critical cell types that trigger and contribute to fibrosis in this depot are not completely understood. Whether adipose mesothelial cells (AMCs) play a role in pathologic obesity has been unclear.

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Project description:Obesity causes the change of microenvironment of adipose tissue and induces the occurrence of adipose tissue inflammation. The objective of this study was to analyze the internal mechanism of microenvironment change in mouse parepididymal adipose tissue by single-nucleus RNA sequencing. Nutritional obesity mouse model was established and verified by morphology, blood index and liver oil red O staining. Select Ctrl group, Mid_Ob group and Ob group, and take 8 mice at 3 time points. The changes of cell population, gene and signaling pathway expression in the adipose tissue of the parastriatic muscle in mice during obesity were detected by single-nucleus RNA sequencing and immunohistochemistry. According to the results of single-nucleus RNA sequencing, adipose tissue was divided into fibroblasts, macrophages, neutrophils and endothelial cells. It is found that all cell types have changes during the development of obesity and play an important role in regulating the microenvironment of adipose tissue.

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PDGFRα+ not CD137+ progenitors control visceral obesity via glucocorticoid mediated TEAD1 methylation state

Project description:summary:Glucocorticoids have impact on visceral obese which crucial contributor to the burden of obesity complications. Subcutaneous and visceral adipose have the heterogeneity of cellular populations. However, the mechanism of glucocorticoids mediated depot-specific regulation remains unclear. Here, we report PDGFRα+ progenitors, dominated in visceral adipose which can convert to white-typical adipocytes, are glucocorticoid-sensitive progenitors. While CD137+ progenitors, mainly harbored in subcutaneous adipose, which are beige-typical adipocytes, are glucocorticoid-passivated progenitors. Mechanistically, we proved that Glucocorticoids elevate TEAD1, transcriptional coactivator of glucocorticoid receptor, by down-regulating the methylation states in PDGFRα+ progenitors. TEAD1 bonds the accessible binding sites in miR-27b promoter region and transcriptionally increases miR-27b expression which previously proved to be the browning ability inhibitor in human and rodent white adipose. These data provide insight into the mechanism of glucocorticoids mediation of visceral obesity and the pathophysiology of depot-specific variations of high fat diet induced obesity.

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