Expression data from the adipose-derived mesenchymal stem cell (ASCs) line
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ABSTRACT:
PROVIDER: PRJNA1151077 | ENA |
REPOSITORIES: ENA
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Project description:We investigated the differentiation of adipose-derived stem cell line (ASCs) into keratinocyte-like cells in the presence of the competitive Rab7 inhibitor, CID-1067700 We utilized microarrays to pinpoint distinct categories of genes that are either up-regulated or down-regulated, and to clarify the regulatory pathways affected by Rab7 inhibition in ASCs.
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Project description:Cytoskeletal tension is an intracellular mechanism through which cells convert a mechanical signal into a biochemical response, including production of cytokines and activation of various signaling pathways. Adipose-derived stromal cells (ASCs) were allowed to spread into large cells by seeding them at a low-density (1,250 cells/cm2), which was observed to induce osteogenesis. Conversely, ASCs seeded at a high-density (25,000 cells/cm2) featured small cells that promoted adipogenesis. RhoA and actin filaments were altered by changes in cell size. Blocking actin polymerization by Cytochalasin D influenced cytoskeletal tension and differentiation of ASCs. To understand the potential regulatory mechanisms leading to actin cytoskeletal tension, cDNA microarray was performed on large and small ASCs. Connective tissue growth factor (CTGF) was identified as a major regulator of osteogenesis associated with RhoA mediated cytoskeletal tension. Subsequently, knock-down of CTGF by siRNA in ASCs inhibited this osteogenesis. Therefore, we conclude that cytoskeletal tension is important for CTGF-regulated ASC osteogenic differentiation. Computed
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Project description:Human adipose tissue contains two populations of progenitors (EPCs and ASCs) with cooperative roles in breast cancer. EPCs (CD45-CD34+CD31+CD13-CCRL2+) can generate endothelial cells. ASCs (CD45-CD34+CD31-CD13+CD140b+) are mesenchymal progenitors which generated pericytes. CD13+ cells and CD13- cells from 7 Lipotransfer aspirate
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2019-10-03 | GSE138311 | GEO
Project description:Cytoskeletal tension is an intracellular mechanism through which cells convert a mechanical signal into a biochemical response, including production of cytokines and activation of various signaling pathways. Adipose-derived stromal cells (ASCs) were allowed to spread into large cells by seeding them at a low-density (1,250 cells/cm2), which was observed to induce osteogenesis. Conversely, ASCs seeded at a high-density (25,000 cells/cm2) featured small cells that promoted adipogenesis. RhoA and actin filaments were altered by changes in cell size. Blocking actin polymerization by Cytochalasin D influenced cytoskeletal tension and differentiation of ASCs. To understand the potential regulatory mechanisms leading to actin cytoskeletal tension, cDNA microarray was performed on large and small ASCs. Connective tissue growth factor (CTGF) was identified as a major regulator of osteogenesis associated with RhoA mediated cytoskeletal tension. Subsequently, knock-down of CTGF by siRNA in ASCs inhibited this osteogenesis. Therefore, we conclude that cytoskeletal tension is important for CTGF-regulated ASC osteogenic differentiation.
2011-01-16 | GSE19924 | GEO
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Project description:Objective: Assuming that mesenchymal stem cells adapt to the osteoarthritic joint environment to exert a chondroprotective effect, we aimed at investigating the molecular response set up by MSCs after priming by OA chondrocytes in cocultures. Design: We used primary human OA chondrocytes and adipose stem cells (ASCs) in mono- and cocultures and performed a high throughput secretome analysis. Among secreted proteins differentially induced in cocultures, we identified thrombospondin-1 (THBS1) as a potential candidate that could be involved in the chondroprotective effect of ASCs. Results: Secretome analysis revealed significant induction of THBS1in ASCs/chondrocytes cocultures at the mRNA and protein levels. Interestingly, we showed that THBS1 was up-regulated at late stages of MSC chondrogenic differentiation while recombinant THBS1 exerted a prochondrogenic effect on MSC. However, down-regulation of THBS1 in ASCs did not revert OA chondrocyte phenotype by decreasing hypertrophic and inflammatory markers. Nevertheless, down-regulation of THBS1 in ASCs reduced their immunosuppressive activity while recombinant THBS1 exerted an anti-inflammatory role on T lymphocytes. THBS1 function was evaluated in vivo in the collagenase-induced OA (CIOA) model by comparing ASCs expressing siTHBS1 and control ASCs. The OA protective effect of ASCs was reversed when THBS1 was down-regulated in ASCs indicating that THBS1 plays a role in the therapeutic effect of ASCs Conclusions: Our data gather some evidence that THBS1 exerts a pro-chondrogenic and anti-inflammatory function in vitro, which could partially explain a chondroprotective effect of ASCs in OA.
2018-10-22 | PXD008146 | Pride
Project description:Adipose-derived mesenchymal stem cells (ASCs) are expected to be a new therapy to prevent progression of renal fibrosis; however, they were reported to have procoagulant activity, raising concerns about thrombogenic risk. Thrombomodulin (TM) acts as an anticoagulant factor by binding to thrombin, leading to the hypothesis that ASCs overexpressing TM (TM-ASCs) could be safely used for cell therapy by reducing the risk of thromboembolism. Overexpression of TM using adeno-associated virus (AAV) reduced rat deaths related to renal infarction and pulmonary embolism induced by ASCs. Interestingly, TM-ASCs alleviated renal inflammation and fibrosis potently in ischemia-reperfusion injury (IRI) rats. The therapeutic mechanism of TM-ASCs involved increased prostaglandin E2 (PGE2) secretion, a shift in the macrophage phenotype to immunosuppressive M2 in vitro, and potent M2 macrophage polarization in the damaged areas in vivo. We produced ASCs with enhanced TM expression by pretreatment with a selective inhibitory kappa-B kinase-β (IKKβ) inhibitor. These ASCs also improved thrombotic mortality and markedly attenuated renal fibrosis induced by IRI, similar to TM-ASCs generated by AAV. ASCs with enhanced TM expression by IKKβ also increased PGE2 secretion, leading to a more pronounced polarization of M2 macrophages. Taken together, ASCs with enhanced TM expression eliminated the risk of thrombosis and reinforced therapeutic efficacy. These ASCs might become a standard cellular therapy for renal fibrosis via the intravascular injection of mesenchymal stem cells in the future.
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