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ABSTRACT:
PROVIDER: PRJNA824665 | ENA |
REPOSITORIES: ENA
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Project description:Human bone marrow derived mesenchymal stromal cells (BMSCs) represent a putative cell source candidate for tissue engineering based strategies to repair cartilage and bone. However, traditional isolation of BMSCs by their preference to adhere to plastic leads to very heterogeneous cell populations and may account for high inter-donor variability and unpredictability of chondrogenic differentiation out-come. Identification of a cell fraction with higher chondrogenic capacity and reduced variance in basic chondrogenic differentiation could further aid the process for developing BMSC-based cartilage and bone regeneration approaches. Since single cell derived clones isolated from fresh bone marrow aspirates show a broad range of chondrogenic capacity, we assessed whether the gene expression profile of clones with high and low chondrogenic capacity differs. While a clustering between high and low chondrogenic capacity clones was observed for one donor, donor-to-donor variability drastically hampered the possibility to achieve conclusive results when different donors were considered. NCAM1/CD56 as identified by the transcriptomic analysis of one donor was still up-regulated in clones with higher chondrogenic capacity and we showed that enriching expanded multiclonal BMSCs for CD56+ expression led to an increase in chondrogenic capacity, though still highly affected by donor-to-donor variability. Our study finally suggests that the definition of predictive marker(s) for BMSCs chondrogenesis is challenged by the high donor’s heterogeneity of these cells. Moreover, we hypothesis that multiple pathways may be involved in determining the chondrogenic potential of BMSCs, making the identification of putative markers still an open issue.
2020-01-13 | GSE111822 | GEO
Project description:To further reveal key mRNAs deciding osteogenic, adipogenic, and chondrogenic differentiation of rat bone marrow mesenchymal stem cells (BMSCs) in early phases, we have employed next-generation high-throughput transcriptome sequencing to detect the expression of mRNA in rat BMSCs during differentiation.
2021-10-23 | GSE185140 | GEO
Project description:To clarify the important signaling pathways, SE-lncRNAs, and mRNAs associated with SE-lncRNAs regulating chondrogenic differentiation of BMSCs, we assessed the expression of SE-lncRNAs and mRNAs in three pairs of non-induced and the corresponding induced chondrogenic differentiation human Bone marrow-derived mesenchymal stem cells samples by using Human Super-Enhancer LncRNA Microarray. A total of 77 SE-lncRNAs were identified with 47 SE-lncRNAs upregulated and 30 SE-lncRNAs downregaulated as chondrogenic differentiation. 308 mRNAs were identified with 245 mRNAs upregulated and 63 mRNAs downregulated. Some pathways, such as the focal adhesion, extracellular matrix (ECM)-receptor interaction, TGF-b signaling pathway, and PI3K-Akt signaling pathway, were identified as the key pathways may be involved in the chondrogenic differentiation of BMSCs. Moreover, 5 potentially core regulatory mRNAs (PMEPA1, ENC1, TES, CDK6, ADIRF) and 37 SE-lncRNAs in chondrogenic differentiation were revealed by bioinformatic analysis.
2021-10-06 | GSE171106 | GEO
Project description:Mutations in the RMRP gene are the origin of cartilage-hair hypoplasia. Cartilage-hair hypoplasia is associated with severe dwarfism caused by impaired skeletal development. However, it is not clear why mutations in the RMRP gene lead to skeletal dysplasia. Viperin is a known substrate of RMRP. Since chondrogenic differentiation of the growth plate is required for development of the long bones, we hypothesized that viperin functions as a chondrogenic regulator downstream of RMRP. Viperin protein is expressed throughout the stages of chondrogenic differentiation in vivo. Viperin gene expression is increased during knockdown of Rmrp RNA in the ATDC5 model for chondrogenic differentiation. Viperin is expressed during ATDC5 chondrogenic differentiation. Viperin knockdown reduces, while viperin overexpression increases overall protein secretion, with CXCL10 identified as a potential target via mass spectrometry-proteomics. CXCL10 protein expression is reduced during knockdown and increased during overexpression of viperin and CXCL10 protein expression coincides with viperin expression in ATDC5 chondrogenic differentiation. Viperin knockdown induces, while viperin overexpression reduces TGFβ activity. Furthermore, viperin knockdown conditioned media increases, while viperin overexpression conditioned media reduces chondrogenic differentiation of ATDC5 cells. TGFβ target genes Pai1 and Smad7 are increased during knockdown and reduced during overexpression of viperin. Moreover, TGFβ activity is reduced when differentiating ATDC5 cells are exposed to CXCL10 and, acting as a viperin overexpression mimic, CXCL10 similarly reduces chondrogenic differentiation of ATDC5. Lastly, we show that in CHH patient cells, RMRP expression is reduced and viperin expression is increased, coinciding with reduced chondrogenic differentiation and increased CXCL10 expression, possibly explaining the CHH phenotype. Together our data show that viperin may play a pivotal role in chondrogenic differentiation, with potential consequences for cartilage-hair hypoplasia pathobiology.
2019-02-15 | PXD006999 | Pride
Project description:Pathological processes like osteoporosis or steroid-induced osteonecrosis of the hip are accompanied by increased bone marrow adipogenesis. Such disorder of adipogenic/osteogenic differentiation, which affects also bone marrow derived mesenchymal stem cells (BMSCs) contributes to bone loss during aging. Therefore, we investigated the effects of extracellular vesicles (EVs) isolated from human (h)BMSCs during different stages of osteogenic differentiation on osteogenic and adipogenic differentiation capacity of naïve hBMSCs.
2022-10-14 | PXD035845 | Pride
Project description:Previously we have shown that the snoRNA RMRP is differentially expressed during chondrogenic differentiation and interference with its function led to important changes in the outcome of chondrogenic differentiation with consequences for ribosomal RNA levels and human disease. To identify additional snoRNAs that may play a role in chondrogenic differentiation, we performed small RNA sequencing (<200 nt) in ATDC5 chondrogenic differentiation at day 0, 7 and 14.
2022-05-01 | E-MTAB-10529 | biostudies-arrayexpress
Project description:To identify microRNAs which differentially expressed in the BMSCs of aged and young mice and and investigate its influences on BMSCs differentiation with ageing. The microRNAs expressions of BMSCs from 3 aged mice and 3 young mice were measured.
2014-04-29 | E-GEOD-57127 | biostudies-arrayexpress
Project description:To identify microRNAs which differentially expressed in the BMSCs of aged and young mice and and investigate its influences on BMSCs differentiation with ageing.
2014-04-29 | GSE57127 | GEO
Project description:Introduction: In addition to the well-known cartilage extracellular matrix-related expression of Sox9, we demonstrated that chondrogenic differentiation of progenitor cells is driven by a sharply defined bi-phasic expression of Sox9: an immediate early and a late (extracellular matrix associated) phase expression. In this study we aimed to determine what biological processes are driven by Sox9 during this early phase of chondrogenic differentiation. Materials: Sox9 expression in ATDC5 cells was knocked-down by siRNA transfection at the day before chondrogenic differentiation or at day 6 of differentiation. Samples were harvested at 2 hours, and 7 days of differentiation. The transcriptomes (RNA-seq approach) and proteomes (Label-free proteomics approach) were compared using pathway and network analyses. Total protein translational capacity was evaluated with the SuNSET assay, active ribosomes with polysome profiling and ribosome modus with bicistronic reporter assays. Results: Early Sox9 knockdown severely inhibited chondrogenic differentiation weeks later. Sox9 expression during the immediate early phase of ATDC5 chondrogenic differentiation regulated the expression of ribosome biogenesis factors and ribosomal protein subunits. This was accompanied by decreased translational capacity following Sox9 knockdown, and this correlated to lower amounts of active mono- and polysomes. Moreover, cap- versus IRES-mediated translation was altered by Sox9 knockdown. Sox9 overexpression was able to induce reciprocal effects to the Sox9 knockdown. Conclusion: Here we identified an essential new function for Sox9 during early chondrogenic differentiation. A role for Sox9 in regulation of ribosome amount, activity and/or composition may be crucial in preparation for the demanding proliferative phase and subsequent cartilage extracellular matrix-production of chondroprogenitors in the growth plate in vivo.
2021-06-18 | PXD024715 | Pride