Suppr超能文献

通过 PI3K/Akt 信号通路下调 MT1-MMP 对于机械拉伸抑制骨髓间充质干细胞侵袭是必需的。

MT1-MMP downregulation via the PI3K/Akt signaling pathway is required for the mechanical stretching-inhibited invasion of bone-marrow-derived mesenchymal stem cells.

机构信息

Department of Bioengineering, College of Bioengineering, Chongqing University, Key Laboratory of Biorheological Science and Technology, Ministry of Education, Chongqing, China.

出版信息

J Cell Physiol. 2019 Aug;234(8):14133-14144. doi: 10.1002/jcp.28105. Epub 2019 Jan 19.

Abstract

Mobilization from the bone marrow and the migration of bone-marrow-derived mesenchymal stem cells (BMSCs) through the peripheral circulation to injured tissue sites are regulated by multiple mechanical and chemical factors. We previously demonstrated that mechanical stretching promotes the migration but inhibits the invasion of BMSCs. However, the involved mechanisms, especially the mechanism of stretching-inhibited BMSC invasion, have not been thoroughly elucidated to date. In this study, we found that mechanical stretching with a 10% amplitude at a 1-Hz frequency for 8 hr significantly reduces BMSC invasion and downregulates the expression of membrane type-1 matrix metalloproteinases (MT1-MMP) at both the messenger RNA and protein levels. The overexpression of MT1-MMP restores mechanical stretching-reduced BMSC invasion. Moreover, phosphatidylinositol 3-kinase (PI3K)-dependent Akt phosphorylation in BMSCs was found to be inactivated by mechanical stretching. Pharmacological inhibitors of PI3K/Akt signaling (LY294002 or A443654) reduced the expression of MT1-MMP and impaired BMSC invasion. In addition, the upregulation of Akt phosphorylation by a pharmacological activator (SC79) increased MT1-MMP expression and suppressed mechanical stretching-reduced BMSC invasion. Taken together, our results suggest that mechanical stretching inhibits BMSC invasion by downregulating MT1-MMP expression by suppressing the PI3K/Akt signaling pathway.

摘要

骨髓动员和骨髓间充质干细胞(BMSCs)通过外周循环迁移到受损组织部位受多种机械和化学因素的调节。我们之前的研究表明,机械拉伸促进了 BMSC 的迁移,但抑制了其侵袭。然而,到目前为止,所涉及的机制,特别是拉伸抑制 BMSC 侵袭的机制,尚未得到彻底阐明。在这项研究中,我们发现,以 1Hz 的频率对细胞施加 10%幅度的拉伸刺激 8 小时,可显著降低 BMSC 的侵袭,并在信使 RNA 和蛋白水平下调膜型 1 基质金属蛋白酶(MT1-MMP)的表达。MT1-MMP 的过表达可恢复机械拉伸降低的 BMSC 侵袭。此外,我们发现机械拉伸会使 BMSCs 中的磷脂酰肌醇 3-激酶(PI3K)依赖性 Akt 磷酸化失活。PI3K/Akt 信号通路的药理学抑制剂(LY294002 或 A443654)可降低 MT1-MMP 的表达并损害 BMSC 的侵袭。此外,药理学激活剂(SC79)可上调 Akt 磷酸化,增加 MT1-MMP 的表达,并抑制机械拉伸降低的 BMSC 侵袭。综上所述,我们的研究结果表明,机械拉伸通过抑制 PI3K/Akt 信号通路下调 MT1-MMP 的表达来抑制 BMSC 的侵袭。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验