Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB17167 | ENA |
REPOSITORIES: ENA
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Project description:We identified a population of obesity-promoted adipogenic preadipocytes that co-expressed Fabp4 and ICAM-1. Fabp4-Cre;mTmG mice were treated with high-fat diet for 16 weeks. The inguinal adipose tissues were collected and digested to obtain vascular and stromal fractions (SVF). The mature adipocytes, CD31-CD45-Sca-1+PDGFR-α+ICAM-1+EGFP+, CD31-CD45-Sca-1+PDGFR-α+ICAM-1+EGFP-, CD31-CD45-Sca-1+PDGFR-α+ICAM-1- cell population were isolated for RNA-seq.
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Project description:The interstitial and perivascular spaces of the heart contain stem-like cells including cardiac colony forming units - fibroblast (cCFU-F), a sub-fraction of SCA1+PDGFR-alpha +CD31- (S+P+) immature stromal cells with the qualities of mesenchymal stem cells, that we have characterized previously. Here we explore the role of platelet-derived growth factor receptor (PDGFR-alpha in cCFU-F and S+P+ cell niche regulation in homeostasis and repair. PDGFR-alpha signaling modulated quiescence, metabolic state, mitogenic propensity and colony formation, as well as the rate and stability of self-renewal. Exogenously administered PDGF-AB ligand had anti-aging effects on cCFU-F, akin to those seen in heterochronic parabiotic mice. Post-myocardial infarction (MI), PDGF-AB stimulated S+P+ cell proliferation and conversion to myofibroblasts through a metabolic priming effect, yet significantly enhanced anatomical and functional repair via multiple cellular processes. Our study provides a rationale for a novel therapeutic approach to cardiac injury involving stimulating endogenous repair mechanisms via activation of cardiac stem and stromal cells.
2019-11-01 | GSE106779 | GEO
Project description:The interstitial and perivascular spaces of the heart contain stem-like cells including cardiac colony forming units - fibroblast (cCFU-F), a sub-fraction of SCA1+PDGFR-alpha +CD31- (S+P+) immature stromal cells with the qualities of mesenchymal stem cells, that we have characterized previously. Here we explore the role of platelet-derived growth factor receptor (PDGFR-alpha in cCFU-F and S+P+ cell niche regulation in homeostasis and repair. PDGFR-alpha signaling modulated quiescence, metabolic state, mitogenic propensity and colony formation, as well as the rate and stability of self-renewal. Exogenously administered PDGF-AB ligand had anti-aging effects on cCFU-F, akin to those seen in heterochronic parabiotic mice. Post-myocardial infarction (MI), PDGF-AB stimulated S+P+ cell proliferation and conversion to myofibroblasts through a metabolic priming effect, yet significantly enhanced anatomical and functional repair via multiple cellular processes. Our study provides a rationale for a novel therapeutic approach to cardiac injury involving stimulating endogenous repair mechanisms via activation of cardiac stem and stromal cells.
2019-11-01 | GSE106778 | GEO
Project description:Kidney fibrosis is characterized by expansion and activation of platelet-derived growth factor receptor-β (PDGFR-β) positive mesenchymal cells. To study the consequences of PDGFR-ß activation, we developed a model of primary renal fibrosis using transgenic mice with PDGFR-β activation specifically in renal mesenchymal cells, driving their pathological proliferation and phenotypic switch towards myofibroblasts. This resulted in progressive mesangioproliferative glomerulonephritis, mesangial sclerosis and interstitial fibrosis with progressive anemia due to loss of erythropoietin production by fibroblasts. We used microarrays to compare wildtype animals (Foxd1_wt Pdgfrb_wt) to animals with constitutive mesenchymal PDGFR-β activation (Foxd1_mt Pdgfrb V536A) in the kidney to identify target genes of PDGFR-β signaling.
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Project description:This study investigates the effects of hyperbaric oxygen (HBO) on cellular senescence and aging-related phenotypes. In naturally aged mice, HBO treatment reduced systemic senescence burden and reversed aging-related transcriptomic signatures in skin, liver, and kidney tissues. Additionally, single-session HBO exposure was shown to preferentially suppress SASP propagation in human stromal cells. This dataset includes transcriptomic profiles of skin, liver, and kidney tissues from young, aged, and HBO-treated aged mice, as well as human primary prostate stromal cells (PSC27).
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Project description:Bulk RNA-seq of CD248+/- PDGFR-α+ cardiac fibroblasts
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Project description:Aging and the chronic diseases associated with aging have become a great burden to modern society. Recent animal studies on heterochronic parabiosis have revealed that young blood has a powerful rejuvenating effect on aged tissues, but which components of the young blood are responsible for the rejuvenating effects remains unclear. In this study, we found that small extracellular vesicles (sEVs) purified from the plasma of young mice could counteract pre-existing aging at the molecular, mitochondrial, cellular and physiological levels. In detail, injection of young sEVs into aged mice extended lifespan, attenuated senescent phenotypes and mitigate age-associated impairments on various tissues (hippocampus, muscle, heart, testis, bone, etc). Mechanistical studies using iTRAQ-based quantitative proteomic analyses combined with GO term cluster revealed that the altered proteomes in aged tissues of young sEVs-treated mice were specifically related to their roles in regulating cellular senescence, metabolic process, epigenetic modification, genomic stability, etc, which are the cardinal features associated with aging. Particularly, the sEVs derived from young mice and young human donors could stimulate PGC-1α (a master regulator of mitochondrial biogenesis and energy metabolism) expression in vitro and in vivo through their rejuvenating miRNA cargos, thereby facilitating mitochondrial regeneration and counteracting mitochondrial deficits in aged tissues. Taken together, this study demonstrates that young sEVs can reverse degenerative changes and age-related dysfunctions through stimulating PGC-1α expression and regenerating intact mitochondria.
2024-03-31 | PXD030350 | Pride
Project description:Platelet-derived growth factor receptor (PDGFR) signaling plays an important role in the embryonic formation of many different tissues. There is a family of PDGF isoforms which signal through the PDGF receptors α (PDGFRα) and β (PDGFRβ). PDGF regulates many key cellular processes of mesenchymal cell function including proliferation, differentiation, migration and extracellular matrix (ECM) synthesis. While PDGF has been used to enhance flexor tendon healing in vivo, its role in postnatal tendon growth has remained largely unexplored. To determine the importance of PDGFR signaling in postnatal tendon growth, we performed pharmacological blockade of PDGFRα and PDGFRβ, and then induced tendon growth via mechanical overload using the hindlimb synergist ablation model. Our hypothesis was that inhibition of PDGFR signaling will restrict normal growth of tendon tissue in response to mechanical loading.
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Project description:Mass spectrometry analysis of NeuN-positive neuronal nuclei from cortices of young and aged mice
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