Li Yang, Shi Xu, Yang Liming, Mou Yan, Li Yingbo, Dang Rongjing, Li Changyuan
Department of Thoracic Surgery, The First Hospital of Jilin University, Changchun 130000, Jilin Province, China.
Central Laboratory, The First Hospital of Jilin University, Changchun 130000, Jilin Province, China.
Gene. 2017 Sep 30;630:68-75. doi: 10.1016/j.gene.2017.08.006. Epub 2017 Aug 5.
Mesenchymal stem cells (MSCs) are well recognized for their ability to differentiate into type II alveolar epithelial (ATII) cells in damaged lungs, which is critical for reepithelization and recovery in acute lung injury (ALI). However, the high level of transforming growth factor-β (TGF-β) commonly seen in injured lung tissues is also able to induce MSCs to differentiate into fibroblast-like cells. In this study, we found that hypoxia could promote umbilical cord mesenchymal stem cells (UCMSCs) differentiation into ATII cells rather than into fibroblast-like cells, and this effect was mainly mediated by microRNA-145 (miR-145), which could induce the inhibition of TGF-β signaling by targeting TGF-β receptor II (TGFβRII). Clarifying the function of hypoxia in the fate determination of MSCs is important for improving stem cell-based therapies for ALI.
间充质干细胞（MSCs）因其在受损肺组织中分化为II型肺泡上皮（ATII）细胞的能力而广为人知，这对于急性肺损伤（ALI）的再上皮化和恢复至关重要。然而，在受伤肺组织中常见的高水平转化生长因子-β（TGF-β）也能够诱导MSCs分化为成纤维细胞样细胞。在本研究中，我们发现缺氧可促进脐带间充质干细胞（UCMSCs）分化为ATII细胞而非成纤维细胞样细胞，并且这种作用主要由微小RNA-145（miR-145）介导，miR-145可通过靶向TGF-β受体II（TGFβRII）诱导TGF-β信号传导的抑制。阐明缺氧在MSCs命运决定中的作用对于改善基于干细胞的ALI治疗很重要。
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