Gene expression in BMSCs isolated from NONMMUT002667 gene KO mice and wildtype control mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE116926 | GEO | 2018/08/15
REPOSITORIES: GEO
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Project description:Bone marrow stromal cells (BMSCs) provide hematopoietic support, immunoregulation and contain a stem cell fraction capable of skeletogenic differentiation. A heterogeneous population of primary bone marrow BMSCs were isolated from a single human donor (FH181), and a lentiviral expression system was used to overexpress human telomerase reverse transcriptase (hTERT) and generate single cell-derived immortalised BMSC lines for multi-level analysis of functional markers for BMSC subsets. All clones expressed typical BMSC cell surface antigens, however clones Y101 and Y201 displayed typical BMSC tri-lineage differentiation capacity where clones Y102 and Y202 lacked significant tri-lineage differentiation potential. High quality RNA samples were isolated from all lines, and global gene expression analysis was performed in triplicate arrays (using Agilent SurePrint G3 Human Gene Expression 8x60K v2 Microarrays) in order to identify distinguishing characteristics of these lines, compared to the parental primary BMSCs from which they were derived.
2015-07-23 | E-MTAB-3511 | biostudies-arrayexpress
Project description:Gene expression in BMSCs isolated from NONMMUT002667 gene KO mice and wildtype control mice
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Project description:Steroid-induced avascular necrosis of the femoral head (SANFH) is closely associated with the imbalance between adipogenic and osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). Additionally, epigenetic regulation plays a critical role in this process. Our previous research found that during BMSC adipogenic differentiation, C/EBPα enhances the histone H3K27 acetylation modification at the PPARγ promoter, promoting sustained adipogenic differentiation of BMSCs, suggesting that Histone deacetylases (HDACs) may play an important role in BMSC adipogenic differentiation. However, identifying specific HDAC target genes requires further investigation. This study combines cell experiments with clinical specimen experiments to screen specific HDAC genes involved in BMSC adipogenic differentiation and explore their preliminary functions. Our findings indicate that HDAC10 influences the progression of steroid-induced avascular necrosis of the femoral head by regulating BMSC adipogenic differentiation, possibly through its association with PPARγ histone acetylation. These discoveries provide promising directions for the treatment of steroid-induced avascular necrosis of the femoral head.
2024-04-15 | GSE263681 | GEO
Project description:The proliferation, migration, and osteogenic differentiation of bone mesenchymal stem cells (BMSCs) play vital roles in maintaining bone mass and metabolism. BMSC base cell therapy has become a competitive treatment option for osteoporosis.Small are critical regulators of cellular processes. Small RNA sequencing was used to detect piRNA expression during BMSC proliferation.
2024-06-01 | GSE234060 | GEO
Project description:Abstract Background: Bone marrow stromal cells (BMSCs) are being used for immune modulatory, anti-inflammatory and tissue engineering applications, but the properties responsible for these effects are not completely understood. Human BMSCs were characterized to identify factors that might be responsible for their clinical effects and biomarkers for assessing their quality. Methods: Early passage BMSCs prepared from marrow aspirates of 4 healthy subjects were compared to 3 human embryonic stem cell (hESC) samples, CD34+ cells from 3 healthy subjects and 3 fibroblast cell lines. The cells were analyzed with oligonucleotide expression microarrays with more than 35,000 probes. Results: BMSC gene expression signatures of BMSCs differed from those of hematopoietic stem cells (HSCs), hESCs and fibroblasts. Genes up-regulated in BMSCs were involved with cell movement, cell-to-cell signaling and interaction and proliferation. The BMSC up-regulated genes were most likely to belong to integrin signaling, integrin linked kinase (ILK) signaling, NFR2-mediated oxidative stress response, regulation of actin-based motility by Rho, actin cytoskeletal signaling, caveolar-mediated endocytosis, clathrin-mediated endocytosis and Wnt/beta catenin signaling pathways. Among the most highly up-regulated genes were structural extracellular (ECM) proteins: alpha1 and beta1 integrin chains, fibronectin, collagen type IIIalpha1, and collagen type Valpha1 and functional EMC proteins: connective tissue growth factor (CTGF) and transforming growth factor beta induced protein (TGFBI) and ADAM12. Conclusions: Global analysis of human BMSCs suggests that they are mobile, metabolically active, proliferative and interactive cells that make use of integrins and integrin signaling. They produce abundant ECM proteins; some of which may contribute to their clinical immune modulatory and anti-inflammatory effects. Seven samples from early passage BMSCs were prepared from marrow aspirates of healthy subjects and compared to 3 human embryonic stem cell (hESC) samples, CD34+ cells from 3 healthy subjects and 3 fibroblast cell lines. Total RNA from a pool of PBMCs from six healthy subjects was extracted and amplified into aRNA to serve as a reference.
2011-09-20 | E-GEOD-24871 | biostudies-arrayexpress
Project description:A protocol was established for the derivation of Schwann cell-like cells from human BMSCs. The commitment to the Schwann cell fate was acquired by Schwann cell-like cells in co-culture with rat DRG neurons. Microarray analysis provided evidence that the human BMSC-derived Schwann cells were functionally mature.
2017-08-01 | GSE102049 | GEO
Project description:Abstract Background: Bone marrow stromal cells (BMSCs) are being used for immune modulatory, anti-inflammatory and tissue engineering applications, but the properties responsible for these effects are not completely understood. Human BMSCs were characterized to identify factors that might be responsible for their clinical effects and biomarkers for assessing their quality. Methods: Early passage BMSCs prepared from marrow aspirates of 4 healthy subjects were compared to 3 human embryonic stem cell (hESC) samples, CD34+ cells from 3 healthy subjects and 3 fibroblast cell lines. The cells were analyzed with oligonucleotide expression microarrays with more than 35,000 probes. Results: BMSC gene expression signatures of BMSCs differed from those of hematopoietic stem cells (HSCs), hESCs and fibroblasts. Genes up-regulated in BMSCs were involved with cell movement, cell-to-cell signaling and interaction and proliferation. The BMSC up-regulated genes were most likely to belong to integrin signaling, integrin linked kinase (ILK) signaling, NFR2-mediated oxidative stress response, regulation of actin-based motility by Rho, actin cytoskeletal signaling, caveolar-mediated endocytosis, clathrin-mediated endocytosis and Wnt/beta catenin signaling pathways. Among the most highly up-regulated genes were structural extracellular (ECM) proteins: alpha1 and beta1 integrin chains, fibronectin, collagen type IIIalpha1, and collagen type Valpha1 and functional EMC proteins: connective tissue growth factor (CTGF) and transforming growth factor beta induced protein (TGFBI) and ADAM12. Conclusions: Global analysis of human BMSCs suggests that they are mobile, metabolically active, proliferative and interactive cells that make use of integrins and integrin signaling. They produce abundant ECM proteins; some of which may contribute to their clinical immune modulatory and anti-inflammatory effects.
2011-09-21 | GSE24871 | GEO
Project description:Human bone marrow stromal cells (BMSCs) are key elements of the hematopoietic environment and they play a central role in bone and bone marrow physiology. However, how key BMSC functions are regulated is largely unknown. We analyzed the role of the immediate early response transcription factor EGR1 as key BMSC regulator and found that EGR1 was highly expressed in prospectively-isolated primary BMSCs, downregulated upon culture, and lower in non-CFU-F-containing CD45neg BM cells. Furthermore, EGR1 expression was lower in proliferative regenerating adult and fetal primary cells compared to adult steady-state BMSCs. Accordingly, EGR1 overexpression markedly decreased BMSC proliferation but considerably improved hematopoietic stroma support function as indicated by an increased production of transplantable CD34+CD90+ hematopoietic stem cells in expansion co-cultures. The improvement of BMSC stroma support function was mediated by increased expression of hematopoietic supporting genes, such as VCAM1 and CCL28. On the other hand, EGR1 knockdown increased ROS-mediated BMSC proliferation, and clearly reduced BMSC hematopoietic stroma support potential. These findings thus show that EGR1 is a key BMSC transcription factor with a dual role in regulating proliferation and hematopoietic stroma support function that is controlling a genetic program to coordinate the specific functions of BMSC in their different biological contexts.
2019-06-27 | PXD011767 | Pride
Project description:Ex vivo expansion of Bone Marrow Stromal Cells (BMSC) is required to obtain clinical dose for cellular therapy, and different labs use different confluence in their practice, however, the impacts of 100% confluence on the biological properties of BMSC remain controversial. In this study, we detected the changes occurred to BMSCs when they reached 100% confluence, including viability, population doubling time (PDT), apoptosis, colony formation, immunosuppression, proteins in the culture supernatant, and surface markers; we also performed gene expression profiling and microRNA profiling on 50%, 80% and 100% confluent BMSCs. Our results showed that 100% confluent BMSCs had similar level of immunosuppression to 80% confluent BMSCs; they increased the expression of CD10, CD54, CD106, CD200, TLR4, but decreased CD49f and PODXL; we detected of 39 proteins in the culture supernatant, which displayed different patterns and an increase on the PEDF/VEGF ratio was observed with higher confluence. We identified 26 differentially expressed microRNAs, which were reported to be involved in the proliferation and differentiation of BMSC; and 2708 genes that were involved in extracellular matrix, cell adhesion, immune response and inflammatory response; particularly, angiogenesis inhibitor PEDF, and Wnt Singling inhibitors DKK1, DKK2, and DKK3 were up-regulated by 100% confluent BMSCs. These data suggest that 100% confluent BMSC may retain immunosuppressive activities but have comprised pro-angiogenesis effects. Gene expression profiling on BMSCs of 3 confluences (50%, 80% and 100%) from 5 healthy donors: 09FC37 (n=3), 09FC43 (n=3), 09FC44 (n=3), 09FC45 (n=3), 09FC49 (n=3) as biological repeats.
2015-08-01 | E-GEOD-60525 | biostudies-arrayexpress
Project description:The pathogenesis of osteoporosis (OP) is closely associated with the disrupted balance between osteogenesis and adipogenesis in bone marrow-derived mesenchymal stem cells (BMSCs). We analyzed published single-cell RNA sequencing (scRNA-seq) data to dissect the transcriptomic profiles of bone marrow-derived cells in OP, reviewing 56,377 cells across eight scRNA-seq datasets from femoral heads (osteoporosis or osteopenia n=5, osteoarthritis n=3). Seventeen genes, including carboxypeptidase M (CPM), were identified as key osteogenesis-adipogenesis regulators through comprehensive gene set enrichment, differential expression, regulon activity, and pseudotime analyses. In vitro, CPM knockdown reduced osteogenesis and promoted adipogenesis in BMSCs, while adenovirus-mediated CPM overexpression had the reverse effects. In vivo, intraosseous injection of CPM-overexpressing BMSCs mitigated bone loss in ovariectomized mice. Integrated scRNA-seq and bulk RNA sequencing analyses provided insight into the MAPK/ERK pathway's role in the CPM-mediated regulation of BMSC osteogenesis and adipogenesis; specifically, CPM overexpression enhanced MAPK/ERK signaling and osteogenesis. In contrast, the ERK1/2 inhibitor binimetinib negated the effects of CPM overexpression. Overall, our findings identify CPM as a pivotal regulator of BMSC differentiation, which provide new clues for the mechanistic study of OP.
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