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幹細胞能根治紅斑狼瘡

   

最近有究硏指出,紅斑狼瘡的病人身體內的幹細胞衰老速度比正常的細胞快。在身體中,幹細胞扮演重要的角色,血管的產生是
由幹細胞組織出來的,當幹細胞容易衰老血管便不完整,在紅斑狼瘡常見的問題便是血管的炎症。

血管是由幹細胞產生出來的,幹細胞形成血管內皮細胞和周細胞,幹細胞老化快了便不能產生完整的血管內皮。血管內皮不完整會產生血液的不正常凝固,血液不正常凝固便產生血管的炎症。

紅斑狼瘡的關節炎和腎炎同樣是由血管炎引起。

王啟元醫生

Clin Dev Immunol. 2013;2013:134243. doi: 10.1155/2013/134243. Epub 2013 Sep 16.
p53/p21 Pathway involved in mediating cellular senescence of bone marrow-derived mesenchymal stem cells from systemic lupus erythematosus patients.
Gu Z, Jiang J, Tan W, Xia Y, Cao H, Meng Y, Da Z, Liu H, Cheng C.
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Abstract

Our and other groups have found that bone marrow-derived mesenchymal stem cells (BM-MSCs) from systemic lupus erythematosus (SLE) patients exhibited senescent behavior and are involved in the pathogenesis of SLE. Numerous studies have shown that activation of the p53/p21 pat hway inhibits the proliferation of BM-MSCs. The aim of this study was to determine whether p53/p21 pathway is involved in regulating the aging of BM-MSCs from SLE patients and the underlying mechanisms. We further confirmed that BM-MSCs from SLE patients showed characteristics of senescence. The expressions of p53 and p21 were significantly increased, whereas levels of Cyclin E, cyclin-dependent kinase-2, and phosphorylation of retinoblastoma protein were decreased in the BM-MSCs from SLE patients and knockdown of p21 expression reversed the senescent features of BM-MSCs from SLE patients. Our results demonstrated that p53/p21 pathway played a n important role in the senescence process of BM-MSCs from SLE.