Elucidation of molecular mechanisms involved in the immunomodulatory function of newly developed adipose tissue derived mesenchymal stem cells

阐明新开发的脂肪组织来源的间充质干细胞的免疫调节功能的分子机制

• 批准号: 23659443
• 负责人: MATSUO Seiichi
• 金额: $ 2.41万
• 依托单位: Nagoya University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Challenging Exploratory Research
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23659443/
• 关键词: 幹細胞; 再生医療; 免疫抑制; 脂肪由来間葉系幹細胞; 強皮症; マクロファージ; メタボローム解析; 幹細胞; 再生医療; 免疫抑制; 脂肪由来間葉系幹細胞; 強皮症; マクロファージ; メタボローム解析

We have proven that low serum cultured adipose derived mesenchymal stem cells (LASC) suppress T cell proliferation and induce polarization of macrophages into immunomodulatory M2 type, and that these effects of LASC were much stronger than high serum cultured adipose derived mesenchymal stem cells (HASC) or bone marrow derived mesenchymal stem cells (BM-MSC). Inthis study, we studied the mechanisms involved in the immunosuppressive functionof LASC by comparing with HASC or BM-MSC. We found by neutralization experiment and stimulation experiment that LASC derived PGE2 and IL-6 are necessary for the polarization of M2 macrophages, and that PGE2 function via EP4 receptor.

我们已经证明，低血清培养的脂肪衍生的间质干细胞（LASC）抑制T细胞增殖并诱导巨噬细胞极化为免疫调节M2型，而LASC的这些作用比高血清培养的脂肪糖衍生的脂肪衍生的脂肪衍生的脂肪质质干细胞（HASC）或骨骼骨骼裂纹细胞（BMM）（BMMM）（BMMM）。在这项研究中，我们通过与HASC或BM-MSC进行比较研究了LASC的免疫抑制功能所涉及的机制。我们通过中和实验和刺激实验发现LASC衍生的PGE2和IL-6对于M2巨噬细胞的极化是必需的，并且PGE2通过EP4受体的功能。