Department of Thoracic Oncology, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, PR China.
Mol Ther. 2013 Feb;21(2):456-65. doi: 10.1038/mt.2012.183. Epub 2012 Nov 13.
Radiation-induced lung injury (RILI) presents a common and major obstacle in the radiotherapy of thoracic cancers. The aim of this study was to examine whether RILI could be alleviated by mesenchymal stem cells (MSCs) expressing soluble transforming growth factor-β (TGF-β) type II receptor via an adenovirus (Ad-sTβR). Here, we systemically administered male MSCs into female mice challenged with thoracic irradiation. The data showed that either MSCs or Ad-sTβR transduced MSCs (Ad-sTβR-MSCs) specifically migrated into radiation-injured lung. Ad-sTβR-MSCs obviously alleviated lung injury, as reflected by survival and histopathology data, as well as the assays of malondialdehyde (MDA), hydroxyproline, plasma cytokines, and the expression of connective tissue growth factor (CTGF) and α-smooth muscle actin (α-SMA). Furthermore, MSCs and Ad-sTβR-MSCs could adopt the characteristics of alveolar type II (ATII) cells. However, the MSCs levels in the lungs were relatively low to account for the noted therapeutic effects, suggesting the presence of other mechanisms. In vivo, MSCs-conditioned medium (MSCs CM) significantly attenuated RILI. In vitro, MSCs CM protected ATII cells against radiation-induced apoptosis and DNA damage, and modulated the inflammatory response, indicating the beneficial effects of MSCs are largely due to its paracrine activity. Our results provide a novel insight for RILI therapy that currently lack efficient treatments.
放射性肺损伤 (RILI) 是胸部癌症放射治疗中常见且主要的障碍。本研究旨在探讨表达可溶性转化生长因子-β (TGF-β) Ⅱ型受体的间充质干细胞 (MSCs) 通过腺病毒 (Ad-sTβR) 是否能减轻 RILI。在这里,我们将雄性 MSCs 系统地注入到接受胸部照射的雌性小鼠中。数据表明,无论是 MSCs 还是转导 Ad-sTβR 的 MSCs (Ad-sTβR-MSCs) 都能特异性地迁移到放射性损伤的肺中。Ad-sTβR-MSCs 明显减轻了肺损伤,这反映在生存和组织病理学数据,以及丙二醛 (MDA)、羟脯氨酸、血浆细胞因子和结缔组织生长因子 (CTGF) 和α-平滑肌肌动蛋白 (α-SMA) 的表达测定中。此外,MSCs 和 Ad-sTβR-MSCs 可以采用肺泡 II 型 (ATII) 细胞的特征。然而,肺中的 MSCs 水平相对较低,不足以说明其显著的治疗效果,这表明存在其他机制。在体内,MSCs 条件培养基 (MSCs CM) 显著减轻了 RILI。在体外,MSCs CM 可保护 ATII 细胞免受辐射诱导的凋亡和 DNA 损伤,并调节炎症反应,表明 MSCs 的有益作用主要归因于其旁分泌活性。我们的研究结果为目前缺乏有效治疗方法的 RILI 治疗提供了新的见解。