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间充质干细胞移植通过转化生长因子-β信号传导依赖性减轻葡聚糖硫酸钠诱导的结肠炎

TGF-beta signaling-dependent alleviation of dextran sulfate sodium-induced colitis by mesenchymal stem cell transplantation.

作者信息

Wang Chong, Chen Jing, Sun Ling, Liu Yanfang

机构信息

Department of Hematology, The First Affiliated Hospital of Zhengzhou University, 1 Construction East Road, Zhengzhou, 450052, Henan Province, China.

出版信息

Mol Biol Rep. 2014 Aug;41(8):4977-83. doi: 10.1007/s11033-014-3364-6. Epub 2014 Apr 16.

DOI:10.1007/s11033-014-3364-6
PMID:24737572
Abstract

Alleviation of dextran sulfate sodium (DSS)-induced colitis was shown after by transplantation of bone marrow derived cells in mice. Nevertheless, the underlying mechanism remains elusive. In the present study, we transplanted primary mouse mesenchymal stem cells (MSC) into isogeneic mice with DSS-induced colitis. We found that MSC transplantation significantly alleviated the DSS-induced colitis. Inhibition of transforming growth factor beta (TGF-beta) signaling abrogated the therapeutic effect of MSC transplantation on DSS-colitis, suggesting a TGF-beta signaling-dependent manner. Moreover, MSC transplantation seemed to induce M2 macrophage polarization, which appeared to be the major source of TGF-beta in this model. Our data thus demonstrate that MSC transplantation may activate TGF-beta signaling pathways to promote the recovery of DSS-colitis.

摘要

在小鼠中,通过移植骨髓来源的细胞可减轻硫酸葡聚糖钠(DSS)诱导的结肠炎。然而,其潜在机制仍不清楚。在本研究中,我们将原代小鼠间充质干细胞(MSC)移植到患有DSS诱导结肠炎的同基因小鼠体内。我们发现,MSC移植显著减轻了DSS诱导的结肠炎。抑制转化生长因子β(TGF-β)信号通路消除了MSC移植对DSS结肠炎的治疗效果,提示其以TGF-β信号依赖的方式发挥作用。此外,MSC移植似乎诱导了M2巨噬细胞极化,而这似乎是该模型中TGF-β的主要来源。因此,我们的数据表明,MSC移植可能激活TGF-β信号通路以促进DSS结肠炎的恢复。

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Mesenchymal Stem Cell-Macrophage Crosstalk and Maintenance of Inflammatory Microenvironment Homeostasis.间充质干细胞与巨噬细胞的相互作用及炎症微环境稳态的维持
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