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Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue_isoproterenol treatment

ABSTRACT: Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue_isoproterenol treatment

PROVIDER: PRJNA717303 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14073319.fastq.gz	Fastqsanger.gz
	SRR14073320.fastq.gz	Fastqsanger.gz
	SRR14073321.fastq.gz	Fastqsanger.gz
	SRR14073322.fastq.gz	Fastqsanger.gz
	SRR14073323.fastq.gz	Fastqsanger.gz

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Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue

Project description:Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue

| PRJNA698817 | ENA

Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue

Project description:The physiological adaptation to cold environmental temperatures involves the remodeling of energy-storing white adipose tissue (WAT) into an energy-burning thermogenic phenotype, characterized by the emergence of multi-locular beige adipocytes. To date, the full array of cold-responsive cells within WAT that mediate thermogenic remodeling remain undefined. Here, we demonstrate that distinct perivascular PDGFRb+ adipocyte precursor cell (APC) subpopulations are differentially sensitive to cold temperatures in vivo. One day of cold exposure elicits striking transcriptional changes in DPP4+ PDGFRb+ APCs, whereas committed DPP4- PDGFRb+ preadipocytes appear comparatively much less responsive. This adaptation includes beta-adrenergic receptor mediated induction in the expression of the pro-thermogenic cytokine, IL-33. DPP4+ PDGFRb+ cells represent the sole source of IL-33 within inguinal WAT of adult mice. Doxycycline-inducible deletion of Il33 in PDGFRb+ cells at the onset of cold exposure significantly compromises the thermogenic remodeling of WAT without directly impacting the differentiation capacity of APCs per se. Together, these studies reveal the presence of a cold-responsive progenitor cell subpopulation in adult WAT and highlight their ability to regulate tissue plasticity through the production of immunological factors.

2021-11-09 | GSE165974 | GEO

Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue_isoproterenol treatment

2021-11-09 | GSE169672 | GEO

Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue_p-CREB ChIP seq

2021-11-09 | GSE169669 | GEO

Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue_p-CREB ChIP seq

Project description:Cold-Responsive DPP4+ Progenitor Cells Facilitate Thermogenic Remodeling of Subcutaneous Adipose Tissue_p-CREB ChIP seq

| PRJNA717298 | ENA

Cold induces a -adrenergicindependent thermogenic gene program in subcutaneous adipose tissue

Project description:Classic brown fat and inducible beige fat both dissipate chemical energy in the form of heat through the actions of mitochondrial uncoupling protein 1. This nonshivering thermogenesis is crucial for mammals as a defense against cold and obesity/diabetes. Cold is known to act indirectly through the sympathetic nervous systems and -adrenergic signaling, but here we report that cold temperature can directly activate a thermogenic gene program in adipocytes independent of -adrenergic signaling.

2018-08-16 | E-MTAB-4526 | biostudies-arrayexpress

Cold induces a β-adrenergic–independent thermogenic gene program in subcutaneous adipose tissue.

Project description:Cold induces a β-adrenergic–independent thermogenic gene program in subcutaneous adipose tissue.

| PRJEB13034 | ENA

Mammary ductal epithelium controls cold-induced adipocyte thermogenic program

Project description:Sympathetic activation during cold exposure increases adipocyte thermogenesis via the expression of mitochondrial protein uncoupling protein 1 (UCP1)1. The propensity of adipocytes to express UCP1 is under a critical influence of the adipose microenvironment and varies between sexes and among various fat depots2-7. Here, we report that cold-induced adipocyte UCP1 expression in a female mouse subcutaneous white adipose tissue (scWAT) is regulated by mammary gland ductal epithelial cells in the adipose niche. Single-cell RNA-sequencing (scRNA-seq) shows that glandular luminal epithelium subtypes express transcripts that encode secretory factors in controlling adipocyte UCP1 expression under cold conditions. We term luminal epithelium secretory factors as “mammokines”. Using whole-tissue immunofluorescence 3D visualization, we reveal previously undescribed sympathetic nerve-ductal points of contact. We show sympathetic nerve-activated mammary ducts limit adipocyte UCP1 expression via lipocalin 2. Both in vivo and ex vivo ablation of mammary ductal epithelium enhances cold-induced scWAT adipocyte thermogenic gene program. Since the mammary duct network extends throughout most scWATs in female mice, females show markedly less scWAT UCP1 expression, fat oxidation, energy expenditure, and subcutaneous fat mass loss compared to male mice, implicating sex-specific roles of mammokines in adipose thermogenesis. These results show a previously uncharacterized role of sympathetic nerve-activated glandular epithelium in adipocyte UCP1 expression and suggest an evolutionary function of mammary duct luminal cells in defending glandular adiposity during cold exposure. Overall, our findings highlight mammary gland epithelium as a highly active metabolic cell type and implicate a broader role of mammokines in controlling female adipose metabolism, mammary gland physiology, and systemic energy homeostasis.

2023-05-01 | GSE231394 | GEO

Changes in gene expression in primary human white preadipocytes in response to knockdown of DPP4

Project description:Transcriptional profiling of primary human white preadipocytes after infection with lentiviral vector either containing shRNA directed against dipeptidypeptidase 4 (DPP4) or unspecific shRNA as negative control Treatment of cells with DPP4 shRNA or control shRNA was done in 4 biological replicates, the first sample of DPP4 KD was hybridized against the first sh-control sample, the second DPP4 smple against the second control sample and so on

2015-11-24 | E-GEOD-75328 | biostudies-arrayexpress

Obesity hinders the efficacy of adipose-derived stem cells for knee osteoarthritis by reducing the proportion of DPP4+ stem cells

Project description:Osteoarthritis (OA) is the most prevalent and disabling joint disease, while adipose-derived stem cells (ASCs) have emerged as a promising therapeutic option in pre-clinical studies. However, the therapeutic efficacy of ASCs may be influenced by the source of these cells, especially in obese patients. This study compared the effects of intra-articular injections of ASCs from wild-type (WT) and ob/ob (OB) mice. Behavioral and histological analyses demonstrated that WT-ASCs significantly alleviated OA symptoms, restoring paw withdrawal thresholds and improving gait parameters while reducing cartilage degradation. In contrast, OB-ASCs only partially improved gait and did not significantly affect cartilage degeneration. Single-cell RNA sequencing of stromal vascular fractions from subcutaneous adipose tissue revealed distinct ASC subpopulations, with DPP4+ cells being notably reduced in obese mice. In vitro, OB-ASCs and high-fat-diet (HFD)-ASCs exhibited impaired proliferation and chondrogenesis but HFD-ASCs retained anti-inflammatory properties. Further investigation using fluorescence-activated cell sorting (FACS) isolated DPP4+ and DPP4- ASCs from WT mice, demonstrating that DPP4+ cells had superior chondrogenic potential and reduced OA pain more effectively than DPP4- cells. These findings suggest that obesity impairs the therapeutic potential of ASCs in OA, primarily due to reduced proliferation and chondrogenesis, and highlight DPP4+ ASCs as a promising candidate for cell therapy in OA.

2025-03-16 | GSE291456 | GEO

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