含纤维连接蛋白III型结构域4通过黏附激酶促进牛骨骼肌源卫星细胞的迁移和分化。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2020-12-01 DOI:10.1080/19336918.2020.1810508
Zhao Wang, Zhiqi Wang, Yusheng Pang, Huili Tong, Yunqin Yan, Shuang Li, Shufeng Li
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引用次数: 4

摘要

FNDC4是一种改变巨噬细胞活化状态的抗炎因子;它被用来治疗小鼠结肠炎。然而,其在肌肉形成中的作用和功能机制尚不清楚。我们发现FNDC4促进牛MDSCs的迁移和分化。此外,我们报道了它与整合素β1 (ITGβ1)相互作用。由itg - β1介导的FAK调节细胞迁移。我们的结果发现FNDC4影响p-FAK、p-paxillin和vinculin的表达。当FAK的激活形态减少时,过表达或添加FNDC4蛋白不再影响FAK的迁移和分化。因此,我们得出结论,FNDC4通过ITGβ1受体介导的FAK促进牛MDSCs的分化和迁移。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Fibronectin type III domain-containing 4 promotes the migration and differentiation of bovine skeletal muscle-derived satellite cells via focal adhesion kinase.

FNDC4 is an anti-inflammatory factor that alters the activation state of macrophages; it is used to treat colitis in mice. However, its role in muscle formation and mechanism of function remains unknown. We found that FNDC4 promotes the bovine MDSCs migration and differentiation. Furthermore, we reported that it interacts with integrin β1 (ITGβ1). FAK, mediated by ITGβ1, regulates cell migration. Our results found FNDC4 to influence the expression of p-FAK, p-paxillin, and vinculin. Then, overexpressed or added FNDC4 protein could not influence migration and differentiation any more when the activated form of FAK was reduced. Therefore, we concluded that FNDC4 promotes the differentiation and migration of bovine MDSCs via the FAK, mediated by the ITGβ1 receptor.

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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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