Expression data from young and aged BMSCs
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA480646 | ENA |
REPOSITORIES: ENA
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Project description:Bone marrow mesenchymal stem cells (BMSCs) differentiate into various mature cell types, including adipocytes and osteoblasts, which is determined by genetic, molecular mediators and local microenvironment. With age, BMSCs become inclined to undergo differentiation into adipocytes rather than osteoblasts, resulting in an increased number of adipocytes and a decreased number of osteoblasts, causing osteoporosis. The dysregulated the gene expression in BMSCs during aging were analyzed. We used microarrays to detail the global programme of gene expression duing aing in BMSCs.
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Project description:Young and Aged osteocytes in bone matrix secreted plenty of extracellular vesicles (EVs) with different functions. We found that EVs released from aged bone matrix (AB-EVs) during bone resorption favor adipogenesis rather than osteogenesis of BMSCs and augment calcification of vascular smooth muscle cells (VSMCs). In this work, we aim to detect the differential regulation microRNAs. Vascular calcification often occurs with osteoporosis, a contradictory association called “calcification paradox”. We find that extracellular vesicles (EVs) released from aged bone matrix (AB-EVs) during bone resorption favor adipogenesis rather than osteogenesis of BMSCs and augment calcification of vascular smooth muscle cells (VSMCs). Intravenous or intramedullary injection of AB-EVs promotes bone-fat imbalance and exacerbates Vitamin D3 (VD3)-induced vascular calcification in young or old mice. To explore the involvement of miRNAs in the AB-EVs-induced promotion of adipocyte formation and vascular calcification, the Agilent miRNA array was conducted to compare the miRNA expression profiles in AB-EVs and YB-EVs from mouse bone specimens. Our study uncovers the role of AB-EVs as a messenger for calcification paradox by transferring functional miRNAs.
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Project description:Dendritic cells (DCs) are major antigen-presenting cells that play a key role in initiating and regulating innate and adaptive immune responses. DCs are critical mediators of tolerance and immunity. The functional properties of DCs changes with age. The purpose of this study was to define the age-associated molecular changes in DCs by gene array analysis using Affymatrix GeneChips. We identified up and down-regulated gene expression changes in DC from aged donors compared to young donors. Total 9 MoDC RNA samples from four young donors (20-27 years) and five aged donors (77-84 years) were analyzed using Affymetrix HG-U133A_2 Gene Arrays to compare differential gene expression changes in MoDC between aged and young groups
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Project description:We report the gene expression changes in mobilized peripheral blood in aged, young, and aged/young samples cocultured in transwell. Restored samples refer to aged MPB co-cultured with young MPB in the transwell culture
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Project description:Vascular calcification often occurs with osteoporosis, a contradictory association called “calcification paradox”. We find that extracellular vesicles (EVs) released from aged bone matrix (AB-EVs) during bone resorption favor adipogenesis rather than osteogenesis of BMSCs and augment calcification of vascular smooth muscle cells (VSMCs). Intravenous or intramedullary injection of AB-EVs promotes bone-fat imbalance and exacerbates Vitamin D3 (VD3)-induced vascular calcification in young or old mice. To explore the involvement of miRNAs in the AB-EVs-induced promotion of adipocyte formation and vascular calcification, the Agilent miRNA array was conducted to compare the miRNA expression profiles in AB-EVs and YB-EVs from mouse bone specimens. Our study uncovers the role of AB-EVs as a messenger for calcification paradox by transferring functional miRNAs.
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Project description:Age-related impairments in myoblast differentiation may contribute to reductions in muscle function in older adults but the underlying proteostasis processes are not well understood. We investigated young (P6-10) and replicatively aged (P48-50) C2C12 myoblast cultures during early (0h-24h) and late (72h-96h) stages of differentiation using deuterium oxide (D2O) labelling and mass spectrometry. The absolute dynamic profiling technique for proteomics (Proteo-ADPT) was used to quantify the absolute rates of abundance change, synthesis and degradation of individual proteins. Proteo-ADPT encompassed 116 proteins and 74 proteins exhibited significantly (P<0.05, FDR <5 %) different changes in abundance between young and aged cells at early and later periods of differentiation. Young cells exhibited a steady pattern of growth, protein accretion and fusion, whereas aged cells failed to gain protein mass or undergo fusion during later differentiation. Maturation of the proteome was retarded in aged myoblasts at the onset of differentiation, but the proteome appeared to ‘catch up’ with the young cells during the early differentiation period. However, this ‘catch up’ process in aged cells was not accomplished by higher levels of protein synthesis. Instead, a lower level of protein degradation in aged cells was responsible for the elevated gains in protein abundance. Our novel data point to a loss of proteome quality as a precursor to the lack of fusion of aged myoblasts and highlights dysregulation of protein degradation, particularly of ribosomal and chaperone proteins, as a key mechanism that may contribute to age-related declines in the capacity of myoblasts to undergo differentiation.
2023-06-27 | PXD029515 | Pride