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Marrow Mesenchymal Cells (marrow + mesenchymal_cell)

Distribution by Scientific Domains
Medical Sciences85%

Kinds of Marrow Mesenchymal Cells

  • bone marrow mesenchymal cell
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    Selected Abstracts

    Bone marrow mesenchymal cells for haemophilia A gene therapy using retroviral vectors with modified long-terminal repeats

    HAEMOPHILIA, Issue 3 2003
    A. Van Damme
    No abstract is available for this article. [source]

    TNF-, Mediates p38 MAP Kinase Activation and Negatively Regulates Bone Formation at the Injured Growth Plate in Rats,

    JOURNAL OF BONE AND MINERAL RESEARCH, Issue 7 2006
    Fiona H Zhou
    Abstract TNF-, is known to inhibit osteoblast differentiation in vitro and yet it is essential for bone fracture repair. Roles of TNF-, in the bony repair of injured growth plate were examined in young rats treated with a TNF-, antagonist. The results show that TNF-, mediates p38 activation, which influences the recruitment, proliferation, and osteoblast differentiation of mesenchymal cells and negatively regulates bone formation at the injured growth plate. Introduction: TNF-, inhibits expression of osteoblast differentiation factor cbfa1 and osteoblast differentiation in vitro and yet TNF-, signaling is essential for bone fracture healing. Roles of TNF-, in the bony repair of injured growth plate cartilage are unknown. Materials and Methods: Roles of TNF-, in the activation of p38 mitogen activated protein (MAP) kinase and the subsequent bony repair of the injured growth plate were examined in young rats receiving the TNF-, inhibitor ENBREL or saline control. Activation of p38 was determined by Western blot analysis and immunohistochemistry. Inflammatory cell counts on day 1, measurements of repair tissue proportions, and counting of proliferative mesenchymal cells on day 8 at growth plate injury site were carried out (n = 6). Expression of inflammatory cytokines TNF-, and IL-1,, fibrogenic growth factor (FGF)-2, cbfa1, and bone protein osteocalcin at the injured growth plate was assessed by quantitative RT-PCR. Effects of TNF-, signaling on proliferation, migration, and apoptosis of rat bone marrow mesenchymal cells (rBMMCs) and the regulatory roles of p38 in these processes were examined using recombinant rat TNF-,, ENBREL, and the p38 inhibitor SB239063 in cultured primary rBMMCs. Results: p38 activation was induced in the injured growth plate during the initial inflammatory response, and activated p38 was immunolocalized in inflammatory cells at the injury site and in the adjacent growth plate. In addition, activation of p38 was blocked in rats treated with TNF-, antagonist, suggesting a role of TNF-, in p38 activation. Whereas TNF-, inhibition did not alter inflammatory infiltrate and expression of TNF-, and IL-1, at the injured growth plate on day 1, it reduced mesenchymal infiltrate and cell proliferation and FGF-2 expression on day 8. Consistently, TNF-, increased proliferation and migration of rBMMCs in vitro, whereas p38 inhibition reduced rBMMC proliferation and migration. At the injured growth plate on day 8, TNF-, inhibition increased expression of cbfa1 and osteocalcin and increased trabecular bone formation at the injury site. There was a significant inverse correlation between TNF-, and cbfa1 expression levels, suggesting a negative relationship between TNF-, and cbfa1 in this in vivo model. Conclusions: These observations suggest that TNF-, activates p38 MAP kinase during the inflammatory response at the injured growth plate, and TNF-,-p38 signaling seems to be required for marrow mesenchymal cell proliferation and migration at the growth plate injury site and in cell culture. Furthermore, TNF signaling has an inhibitory effect on bone formation at the injured growth plate by suppressing bone cell differentiation and bone matrix synthesis at the injury site. [source]

    Early bone in-growth ability of alumina ceramic implants loaded with tissue-engineered bone

    JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 4 2006
    Yasuaki Tohma
    Abstract To enhance early bonding of an alumina ceramic implant to bone, we evaluated a method of seeding the implant surface with bone marrow mesenchymal cells that differentiated to osteoblasts and bone matrix prior to implantation. The usefulness of the method was evaluated in Japanese white rabbits. In our study, an alumina ceramic test piece loaded with differentiated osteoblasts and bone matrix by a tissue engineering technique was implanted into rabbit bones. Three weeks after the procedure, evaluation of mechanical bonding and histological examination were performed. Histological examination of the noncell-loaded implant surfaces showed no bone infiltration into the implant gap. However, the cell-loaded implant surfaces exhibited new bone infiltration into the implant gap with mechanical bonding. In the mechanical test, the average failure load was 0.60 kgf for the noncell-loaded side and 1.49 kgf for the cell-loaded side. Preculturing mesenchymal cells on the surface of the alumina ceramic prior to implantation increased the debonding strength by two and half times. The present findings indicate early bonding between the implant and bone three weeks after the procedure. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res [source]

    Glucocorticoid-induced differentiation of primary cultured bone marrow mesenchymal cells into adipocytes is antagonized by exogenous Runx2

    APMIS, Issue 8 2010
    LE LIN
    Lin L, Dai S-Dong, Fan G-Yu. Glucocorticoid-induced differentiation of primary cultured bone marrow mesenchymal cells into adipocytes is antagonized by exogenous Runx2. APMIS 2010; 118: 595,605. Long-term clinical use of glucocorticoids often causes the serious side effect of non-traumatic avascular osteonecrosis. The aim of this study was to examine the effects and mechanisms of a glucocorticoid, dexamethasone (Dex), on differentiation of primary cultured rat bone marrow mesenchymal cells (BMCs). We also tried to block the inhibitory effects of Dex on osteoblast differentiation. Adipocyte markers (peroxisome proliferator-activated receptor,-2 and aP2) were increased in response to Dex treatment in a dose- and time-dependent manner, while osteoblastic markers [Runx2, COL 1, osterix, alkaline phosphatase (ALP) and OC] were down-regulated, consistent with ALP and osteocalcin promoter activity. To validate the effects of Runx2 on the expression of osteogenesis and adipocyte genes, pCMV/Flag-Runx2 was transfected into BMCs, and relevant markers were detected after 10,7 M Dex treatment for 48 h. The results indicated that Dex treatment induced adipogenic differentiation and suppressed proliferation. No significant difference was detected in expressions of these genes between Runx2-transfected cells and Dex-treated BMCs. These data suggest that Dex primarily induced adipocyte differentiation of BMCs. Exogenous Runx2 can antagonize the effect of Dex on osteoblast differentiation. [source]

    Development and functional characterization of human bone marrow mesenchymal cells immortalized by enforced expression of telomerase

    BRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2003
    Keichiro Mihara
    Summary. To create immortal mesenchymal cell lines, we transduced primary human bone marrow mesenchymal cells with telomerase reverse transcriptase (TERT). TERT+ mesenchymal cells continued to grow for >,2 years; parallel TERT, cultures underwent senescence after 15 weeks. TERT+ mesenchymal cells did not form foci in soft agar, had a normal karyotype and could differentiate into osteoblasts and chondrocytes. Their capacity to support leukaemic lymphoblasts and normal CD34+ haematopoietic cells was equal to or greater than that of primary cells; 42 TERT+ mesenchymal cell clones varied in their supporting capacity. Immortalized mesenchymal cells offer a promising tool for identifying molecules that regulate human haematopoiesis. [source]