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بیوشیمی مولکولی و سلولی 2013
جزئیات رویداد
همایش ، رویداد ، ژورنال
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  • wnt/β-catenin signaling mediates the senescence of bone marrow-mesenchymal stem cells from systemic lupus erythematosus patients through the p53/p21 pathway

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    • تاریخ ارائه: 1392/07/24
    • تاریخ انتشار در تی پی بین: 1392/07/24
    • تعداد بازدید: 964
    • تعداد پرسش و پاسخ ها: 0
    • شماره تماس دبیرخانه رویداد: -
     recent studies have shown that allogeneic bone marrow (bm)-mesenchymal stem cell transplantation (msct) appears to be effective in systemic lupus erythematosus (sle) patients and lupus-prone mice, contrary to studies in syngeneic bm-msct. these studies indicated that the abnormalities of bm-mscs may be involved in the pathogenesis of sle. our studies and other previous studies have revealed that bm-mscs from sle patients exhibited early signs of senescence, such as flattened morphology, slow proliferation, increased senescence-associated β-galactosidase (sa-β-gal) activity, and so on. however, the mechanisms by which these cells senescences were still unclear. previous studies have demonstrated that wnt/β-catenin signaling plays an important role in stem cell senescence. in the current study, we investigated whether wnt/β-catenin signaling mediates the senescence of bm-mscs from sle patients. we have found that wnt/β-catenin signaling and the p53/p21 pathway were significantly hyperactivated in senescent sle bm-mscs. treatment with 100 ng/ml dickkopf-1 (dkk1), a wnt/β-catenin signaling inhibitor or β-catenin sirna for 48 h could reverse the senescent features of sle bm-mscs. additionally, the expression levels of p53 and p21 were reduced in treated-sle bm-mscs compared with the untreated group. in summary, our study indicated that wnt/β-catenin signaling may play a critical role in the senescence of sle bm-mscs through the p53/p21 pathway.

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