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首页> 外文期刊>Cell biology international. >Suppression of the PI3K-Akt pathway is involved in the decreased adhesion and migration of bone marrow-derived mesenchymal stem cells from non-obese diabetic mice.
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Suppression of the PI3K-Akt pathway is involved in the decreased adhesion and migration of bone marrow-derived mesenchymal stem cells from non-obese diabetic mice.

机译:PI3K-Akt通路的抑制与来自非肥胖糖尿病小鼠的骨髓间充质干细胞的粘附和迁移减少有关。

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摘要

T1DM (type 1 diabetes mellitus) is an autoimmune disease characterized by T-cell-mediated damage of islet beta-cells. The pathology of NOD (non-obese diabetic) mouse involves the insulitis induced by infiltration of T-cells, a similar pathogenic mechanism in T1DM patient. BM-MSCs (bone marrow mesenchymal stem cells) are multipotent progenitor cells that can be isolated from a number of sources. Recent studies have shown that transplantation of MSCs to the NOD mice could prevent the process and have the therapeutic effects on T1DM. In our studies, we have found that migration and adhesion of BM-MSCs from NOD mice were suppressed compared with the BM-MSCs from ICR (imprinting control region) mice, accompanying with the abnormal distribution of FAK (focal adhesion kinase) and F-actin (filamentous actin). Further, we have found that the activation of PI3K (phosphoinositide 3-kinase)-Akt pathway was suppressed in BM-MSCs from NOD mice. When the PI3K-Akt pathway was inhibited by LY294002, the adhesion and migration of BM-MSCs from ICR mice were suppressed as well. These results indicated that the suppression of PI3K-Akt pathway is involved in the decreased adhesion and migration of BM-MSCs from NOD mice.
机译:T1DM(1型糖尿病)是一种自身免疫性疾病,其特征是T细胞介导的胰岛β细胞受损。 NOD(非肥胖型糖尿病)小鼠的病理学涉及由T细胞浸润诱导的胰岛炎,这是T1DM患者的类似致病机制。 BM-MSC(骨髓间充质干细胞)是多能祖细胞,可以从多种来源中分离出来。最近的研究表明,向NOD小鼠移植MSC可以阻止该过程,并对T1DM具有治疗作用。在我们的研究中,我们发现,与ICR(印迹控制区域)小鼠的BM-MSC相比,NOD小鼠的BM-MSC的迁移和粘附受到抑制,并伴有FAK(局灶性粘附激酶)和F-的异常分布肌动蛋白(丝状肌动蛋白)。此外,我们发现在NOD小鼠的BM-MSC中,PI3K(磷酸肌醇3激酶)-Akt途径的激活受到抑制。当LY294002抑制PI3K-Akt途径时,ICR小鼠的BM-MSC的粘附和迁移也受到抑制。这些结果表明,PI3K-Akt途径的抑制与来自NOD小鼠的BM-MSC的粘附和迁移减少有关。

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