Gene expression data from murine bone-marrow osteo and adipo progenitor cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE124905 | GEO | 2019/02/28
REPOSITORIES: GEO
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Project description:Bone marrow stromal cells (BMSCs) were isolated from the femora and tibiae of irtTA-GBD*-TAg transgenic mice. Using cellular cloning we established skeletal progenitors with unipotent osteogenic and adipogenic properties. Previous RNA-seq analysis of more progenitor types revealed differential expression in members of the Interferon-gamma (IFNγ) signaling pathway. Treatment of adipogenic progenitors with IFNγ inhibited adipogenesis and promoted osteogenesis. RNA-seq analysis of osteogenic, adipogenic and IFNγ treated adipogenic clones revealed factors controlling the osteogenic versus adipogenic commitment of bone marrow skeletal progenitors.
2018-07-02 | GSE114475 | GEO
Project description:The healthy growth of adipose tissue depends on the capacity of progenitor cells to undergo denovo adipogenesis. However, the cellular hierarchy and mechanisms governing adipocyteprogenitor differentiation are incompletely understood. Here, we identify a lineage hierarchy25 consisting of distinct mesenchymal cell types present in mouse and human adipose tissue. Cellsmarked by Dpp4 expression are highly proliferative, multipotent progenitors that give rise toIcam1+ committed pre-adipocytes and a related adipogenic population marked by Clec11a andCd142 expression. TGFβ maintains DPP4+ cell identity and inhibits adipogenic commitment ofDPP4+ and CD142+ cells. Intriguingly, DPP4+ progenitors reside in the reticular interstitium that30 envelope many organs including adipose depots. Altogether, this study defines the adipose lineagehierarchy and identifies a new anatomical niche for multipotent mesenchymal progenitors.
2019-05-01 | GSE128890 | GEO
Project description:The healthy growth of adipose tissue depends on the capacity of progenitor cells to undergo denovo adipogenesis. However, the cellular hierarchy and mechanisms governing adipocyteprogenitor differentiation are incompletely understood. Here, we identify a lineage hierarchy25 consisting of distinct mesenchymal cell types present in mouse and human adipose tissue. Cellsmarked by Dpp4 expression are highly proliferative, multipotent progenitors that give rise toIcam1+ committed pre-adipocytes and a related adipogenic population marked by Clec11a andCd142 expression. TGFβ maintains DPP4+ cell identity and inhibits adipogenic commitment ofDPP4+ and CD142+ cells. Intriguingly, DPP4+ progenitors reside in the reticular interstitium that30 envelope many organs including adipose depots. Altogether, this study defines the adipose lineagehierarchy and identifies a new anatomical niche for multipotent mesenchymal progenitors.
2019-05-01 | GSE128891 | GEO
Project description:Physical activity improves overall health and counteracts metabolic pathologies. Adipose tissue and bone are important key targets of exercise; the prevalence of diseases associated with suboptimal physical activity levels has increased in recent times as a result of lifestyle changes. Mesenchymal stem cells (MSCs) differentiation in either osteogenic or adipogenic lineage is regulated by many factors. Particularly, the expression of master genes such as RUNX2 and PPARγ2 is essential for MSC commitment to osteogenic or adipogenic differentiation, respectively. Besides various positive effects on health, some authors have reported stressful outcomes as a consequence of endurance in physical activity. We looked for further clues about MSCs differentiation and serum proteins modulation studying the effects of half marathon in runners by means of gene expression analyses and a proteomic approach. Our results demonstrated an increase in osteogenic commitment and a reduction in adipogenic commitment of MSCs. In addition, for the first time we have analyzed the proteomic profile changes in runners after half-marathon activity in order to survey the related systemic adjustments. Interestingly, proteomic data showed the activation of both inflammatory response and detoxification process. Moreover, the involvement of pathways associated to immune response, lipid transport and coagulation, was elicited. Notably, positive and negative effects may be strictly linked.
2017-09-25 | PXD006704 | Pride
Project description:To further understand mechanisms governing adipogenic fate commitment, we perform a time course transcriptomic study of progenitors at 0, 3, 7 and 14 days post adipogenic induction. The progenitor cells undergo large scale gene expression changes within 3 days of exposure to adipogenic induction and adiponectin expression is strongly induced at day 3. The early detection of ADIPOQ expression suggests fate commitment occurs within 3 days of induction.
2023-04-01 | GSE198481 | GEO
Project description:While the accumulation of bone marrow adipose tissue has been positively associated with aging and high fat diet, the physiological consequences are mostly unknown. It is well established that osteogenic and adipogenic progenitors share a common developmental origin.Unfavorable microenvironmental changes may bias these cell populations towards an adipogenic fate, which in turn could negatively influence bone homeostasis. Our previously collected data from mice reveal a high plasticity of the mesenchymal osteo-adipogenic stem cell population. Therefore, we now wish to perform by RNA-seq in defined cell population with varying adipogenic commitment within this heterogeneous stem cell pool.This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2016-04-11 | E-ERAD-460 | biostudies-arrayexpress
Project description:Background & Aims: Isthmic progenitors, tissue-specific stem cells in the stomach corpus, maintain mucosal homeostasis by balancing between proliferation and differentiation to gastric epithelial lineages. The progenitor cells rapidly adopt an active state in response to mucosal injury. However, it remains unclear how the isthmic progenitor cell niche is controlled during the regeneration of damaged epithelium. Methods: We recapitulated tissue recovery process after acute mucosal injury in the mouse stomach. BrdU incorporation was utilized to trace newly generated cells during the injury and recovery phases. To define epithelial lineage commitment process during recovery, we performed single cell RNA-sequencing on epithelial cells from the mouse stomachs. We validated the effects of amphiregulin (AREG) on the mucosal recovery, utilizing recombinant AREG treatment or AREG deficient mice. Results: We determined that an EGFR ligand, AREG, can control progenitor cell lineage commitment. Based on the identification of lineage-committed subpopulations in the corpus epithelium through single cell RNA-sequencing and BrdU incorporation, we showed that isthmic progenitors give rise to epithelial cell lineages through an ordered paradigm during mucosal regeneration. During recovery, AREG treatment promotes repopulation with parietal cells, while suppressing surface cell commitment of progenitors. In contrast, TGF-alpha did not alter parietal cell regeneration but did induce expansion of surface cell populations. AREG deficiency impairs parietal cell regeneration, but increases surface cell commitment. Conclusions: These data demonstrate that different EGF receptor ligands can distinctly regulate isthmic progenitor-driven mucosal regeneration and lineage commitment.
2026-03-12 | GSE316067 | GEO
Project description:Osteoporosis, a prevalent age-related bone disorder, stems from imbalanced osteoclast/osteoblast activity and skewed mesenchymal stem cell (MSC) lineage commitment. Although lactate is linked to osteoporosis pathogenesis, the role of protein lactylation in MSC osteogenic differentiation remains unelucidated. This experiment explored protein lactylation during early MSC osteogenic differentiation, focusing on histone variant MacroH2A1. Proteomics identified 375–318 lactylated proteins across undifferentiated, osteogenic differentiation Day 3 (OB3), and adipogenic differentiation Day 3 (AD3) MSCs; MacroH2A1 lactylation at lysine 134 (K134) was downregulated in OB3. MacroH2A1(K134Ala) mutation (disrupting lactylation) enhanced MSC osteogenesis. In ovariectomized mice, AAV-MacroH2A1(K134Ala) increased femoral trabecular bone mass and reduced marrow adipose tissue. This experiment demonstrates that MacroH2A1 K134 lactylation regulates MSC osteogenic commitment via epigenetic and transcriptional modulation, offering mechanistic insights and a potential therapeutic target for osteoporosis.
2026-05-24 | GSE331389 | GEO
Project description:We demonstrated the multipotent potential and change of cell identity of human adipose tissue-derived progenitors by subjecting cells to adipogenic, chondrogenic, and osteogenic induction. mRNA transcriptomic profiling results demonstrated the detection of lineage-specific markers.
2023-04-01 | GSE198275 | GEO
Project description:Osteoporosis, a prevalent age-related bone disorder, stems from imbalanced osteoclast/osteoblast activity and skewed mesenchymal stem cell (MSC) lineage commitment. Although lactate is linked to osteoporosis pathogenesis, the role of protein lactylation in MSC osteogenic differentiation remains unelucidated. This experiment explored protein lactylation during early MSC osteogenic differentiation, focusing on histone variant MacroH2A1. Proteomics identified 375–318 lactylated proteins across undifferentiated, osteogenic differentiation Day 3 (OB3), and adipogenic differentiation Day 3 (AD3) MSCs; MacroH2A1 lactylation at lysine 134 (K134) was downregulated in OB3. MacroH2A1(K134Ala) mutation (disrupting lactylation) enhanced MSC osteogenesis. In ovariectomized mice, AAV-MacroH2A1(K134Ala) increased femoral trabecular bone mass and reduced marrow adipose tissue. This experiment demonstrates that MacroH2A1 K134 lactylation regulates MSC osteogenic commitment via epigenetic and transcriptional modulation, offering mechanistic insights and a potential therapeutic target for osteoporosis.
2026-05-30 | GSE331503 | GEO