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Elucidating the impact of chemotherapy on skeletal progenitors [RNA-seq Osteoblast]

ABSTRACT: Mice receiving cyclic doxorubicin (DOX) treatment exhibited long-term skeletal defects. Lineage tracing experiments revealed loss of osteogenesis from bone marrow mesenchymal stem and progenitor cells. We performed molecular characterization on MSPCs to understand the mechanisms underying MSPC dysfunction folloiwng DOX treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE296757 | GEO | 2026/06/15

REPOSITORIES: GEO

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Elucidating the impact of chemotherapy on skeletal progenitors [scRNA-seq]

Project description:Mice receiving cyclic doxorubicin (DOX) treatment exhibited long-term skeletal defects. Lineage tracing experiments revealed loss of osteogenesis from bone marrow mesenchymal stem and progenitor cells. We performed molecular characterization on MSPCs to understand the mechanisms underying MSPC dysfunction folloiwng DOX treatment.

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Murine mesenchymal stem/progenitor cells (MSPC): Ptpn11+/+ MSPC vs. Ptpn11E76K/+ MSPC

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Project description:De novo ASXL1 mutations are found in patients with Bohring-Opitz syndrome, a disease with severe developmental defects and early childhood fatality. The underlying pathologic mechanisms remain largely unknown. Using Asxl1-targeted murine models,we found that Asxl1 global loss or conditional deletion in osteoblasts and their progenitors in mice leads to significant bone loss and markedly decreased numbers of marrow mesenchymal stem/progenitor cells (MSPCs) compared with wild-type (WT) littermates. Asxl1-/- MSPCs displayed impaired self-renewal and skewed differentiation-away from osteoblasts and favoring adipocytes. RNA-seq analysis reveals the altered expression of genes involved in cell proliferation, skeletal development and morphogenesis. Furthermore, gene set enrichment analysis showed a decreased gene expression of stem cell self-renewal signature,suggesting the role of Asxl1 in regulating the stemness of MSPCs. Importantly, introducing Asxl1 normalized NANOG and OCT4 expression and restored the self-renewal capacity of Asxl1-/- MSPCs. Our study unveils a pivotal role of ASXL1 in maintenance of MSPC functions and skeletal development. Examination of mRNA profiles in wild type and Asxl1-/- MSPCs by deep sequencing

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and POT1a deleted MSPCs Transcriptomes.

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