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Discovery and functional assessment of a novel adipocyte population driven by intracellular Wnt/β-catenin signaling in mammals

ABSTRACT: Discovery and functional assessment of a novel adipocyte population driven by intracellular Wnt/β-catenin signaling in mammals

PROVIDER: PRJNA691888 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13428706.fastq.gz	Fastqsanger.gz
	SRR13428707.fastq.gz	Fastqsanger.gz
	SRR13428708.fastq.gz	Fastqsanger.gz
	SRR13428709.fastq.gz	Fastqsanger.gz
	SRR13428710_1.fastq.gz	Fastqsanger.gz

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Discovery and functional assessment of a novel adipocyte population driven by intracellular Wnt/β-catenin signaling in mammals

Project description:Wnt/β-catenin signaling has been well established as a potent inhibitor of adipogenesis. Here, we identified a population of adipocytes that exhibit persistent activity of Wnt/β-catenin signaling, as revealed by the Tcf/Lef-Gfp reporter allele, in embryonic and adult mouse fat depots, named as Wnt+ adipocytes. We showed that this β-catenin-mediated signaling activation in these cells is Wnt ligand- and receptor-independent but relies on AKT/mTOR pathway and is essential for cell survival. Such adipocytes are distinct from classical ones in transcriptomic and genomic signatures and can be induced from various sources of mesenchymal stromal cells including human cells. Genetic lineage-tracing and targeted cell ablation studies revealed that these adipocytes convert into beige adipocytes directly and are also required for beige fat recruitment under thermal challenge, demonstrating both cell autonomous and non-cell autonomous roles in adaptive thermogenesis. Furthermore, mice bearing targeted ablation of these adipocytes exhibited glucose intolerance, while mice receiving exogenously supplied such cells manifested enhanced glucose utilization. Our studies uncover a unique adipocyte population in regulating beiging in adipose tissues and systemic glucose homeostasis.

2021-05-01 | GSE164747 | GEO

Discovery and functional assessment of a novel adipocyte population driven by intracellular Wnt/β-catenin signaling in mammals.

Project description:Wnt/β-catenin signaling has been well established as a potent inhibitor of adipogenesis. Here, we identified a population of adipocytes that exhibit persistent activity of Wnt/β-catenin signaling, as revealed by the Tcf/Lef-GFP reporter allele, in embryonic and adult mouse fat depots, named as Wnt+ adipocytes. We showed that this β-catenin-mediated signaling activation in these cells is Wnt ligand- and receptor-independent but relies on AKT/mTOR pathway and is essential for cell survival. Such adipocytes are distinct from classical ones in transcriptomic and genomic signatures and can be induced from various sources of mesenchymal stromal cells including human cells. Genetic lineage-tracing and targeted cell ablation studies revealed that these adipocytes convert into beige adipocytes directly and are also required for beige fat recruitment under thermal challenge, demonstrating both cell autonomous and non-cell autonomous roles in adaptive thermogenesis. Furthermore, mice bearing targeted ablation of these adipocytes exhibited glucose intolerance, while mice receiving exogenously supplied such cells manifested enhanced glucose utilization. Our studies uncover a unique adipocyte population in regulating beiging in adipose tissues and systemic glucose homeostasis.

| S-EPMC9064292 | biostudies-literature

PGRMC2 is an Intracellular Heme Chaperone Critical for Adipocyte Function

Project description:PGRMC2 is an Intracellular Heme Chaperone Critical for Adipocyte Function

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Beta-catenin stabilization of skin fibroblasts causes fibrotic lesions by preventing adipocyte differentiation of the reticular dermis

2016-01-12 | GSE76751 | GEO

Beta-catenin stabilization of skin fibroblasts causes fibrotic lesions by preventing adipocyte differentiation of the reticular dermis

Project description:The Wnt/alpha-catenin pathway plays a central role in epidermal homeostasis and regeneration but how it affects fibroblast fate decisions is unknown. Here, we investigated the effect of targeted alpha-catenin stabilization in dermal fibroblasts. Comparative gene expression profiling of Sca1- and Sca1+ neonatal fibroblasts, from upper and lower dermis respectively, confirmed that Sca1+ cells had a pre-adipocyte signature and revealed differential expression of Wnt/alphaâ??catenin-associated genes. By targeting all fibroblasts or selectively targeting Dlk1+ lower dermal fibroblasts, we found that ï?¢-catenin stabilization between E16.5 and P2 resulted in a reduction in the dermal adipocyte layer with a corresponding increase in dermal fibrosis and an altered hair cycle. The fibrotic phenotype correlated with a reduction in the potential of Sca1+ fibroblasts to undergo adipogenic differentiation ex vivo. Our findings indicate that Wnt/alpha-catenin signaling controls adipogenic cell fate within the lower dermis, which potentially contributes to the pathogenesis of fibrotic skin diseases. The dermis was separated from back skin of PDGFRAeGFP postnatal pups (P2) by incubation with thermolysin (0.25 mg/ml) (Sigma T7902) overnight at 4Â° and further processed as previously described (Collins et al., 2011). Cells were labeled in PBS + 10% FBS TruStain fcX anti-mouse blocking buffer with the following antibodies: anti-mouse Ly-6A/E (Sca-1)-Alexa Fluor-700 17. Two populations of cells were collected in triplicate. The PDGFRaH2BeGFP/Sca1- and the PDGFRaH2BeGFP/Sca1+. RNA was isolated and prepared for microarray analysis and hybridized to Affymetrix MG430.2A arrays. C, digested in DMEM + 10% FBS containing 2.5 mg/mL collagenase I (Gibco 17100- 017), and further processed

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Adipocyte-derived FABP4 promotes MASLD-induced hepatocellular carcinoma by driving ITGB1-mediated β-catenin activation [rhFABP4]

Project description:Adipocyte-derived FABP4 promotes MASLD-induced hepatocellular carcinoma by driving ITGB1-mediated β-catenin activation [rhFABP4]

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p120-catenin differentially regulates cell migration by Rho-dependent intracellular and secreted signals

Project description:The Adherens Junction protein p120-catenin is implicated in the regulation of cadherin stability, cell migration and inflammatory responses in mammalian epithelial tissues. How these events are coordinated to promote wound repair is not understood. We show that p120-catenin regulates the intrinsic migratory properties or primary mouse keratinocytes, but also influences the migratory behavior of neighboring cells by secreted signals. These events are rooted in the ability of p120-catenin to regulate RhoA-GTPase activity, which leads to a two-tiered control of cell migration. One restrains cell motility via increase of actin stress fibers, reduction in integrin turnover, and an increase in focal adhesions robustness. The other is coupled to the secretion of inflammatory cytokines including Interleukin-24, which causally enhances randomized cell movements. Taken together, our results indicate that p120-RhoA-GTPase-mediated signaling can differentially regulate the migratory behavior of epidermal cells, which has potential implications for chronic wound responses and cancer.

2016-12-31 | GSE55019 | GEO

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