To test the hypothesis that intrinsic renal scattered tubular cells (STC-like cells) contribute to repairing injured tubular epithelial cells (TEC) by releasing extracellular vesicle (EV). EV released from primary cultured pig STC-like cells were confirmed by electron microscopy. Antimycin-A (AMA)-induced injured proximal TEC (PK1 cells) were co-cultured with STC-like cells, STC-like cells-derived EV, or EV-free conditioned-medium for 3 days. Cellular injury, oxidative stress and mitochondrial function were assessed. Transfer of mitochondria from STC-like cells to TEC was assessed using Mito-trackers, and their viability by mitochondrial membrane potential assays. STC-like cells-derived EV were intra-arterially injected into mice 2 weeks after induction of unilateral renal artery stenosis. Two weeks later, renal hemodynamics were studied using magnetic-resonance-imaging, and renal fibrosis assessed ex-vivo. Cultured STC-like cells released EV that were uptaken by TEC. A protective effect conferred by STC-like cells in AMA-induced TEC injury was partly mimicked by their EV. Furthermore, STC-like cells-EV carried and transferred mitochondrial material to injured TEC, which partly restored mitochondrial function. In vivo, STC-like cells-derived EV engrafted in the stenotic kidney, and improved its perfusion and oxygenation. STC-like cells-EV exert protective effects on injured tubular cells in vitro and in vivo, partly by transferring STC-like cells mitochondria, which remain at least partly functional in recipient TEC.

中文翻译：

---

肾散在的肾小管样细胞通过细胞外小泡的释放介导在狭窄的鼠肾中的保护作用。

为了检验这一假设，即内在的肾脏散布性肾小管细胞（STC样细胞）通过释放细胞外囊泡（EV）有助于修复受损的肾小管上皮细胞（TEC）。通过电子显微镜确认从原代培养的猪STC样细胞释放的EV。将抗霉素A（AMA）诱导的受损近端TEC（PK1细胞）与STC样细胞，STC样细胞来源的EV或不含EV的条件培养基共培养3天。评估细胞损伤，氧化应激和线粒体功能。使用线粒体示踪剂评估线粒体从类STC细胞向TEC的转移，并通过线粒体膜电位测定法评估其生存能力。在诱导单侧肾动脉狭窄后2周，将STC样细胞衍生的EV动脉内注射到小鼠体内。两个星期后，使用磁共振成像研究了肾脏血液动力学，并体外评估了肾纤维化。培养的类STC细胞释放出被TEC摄取的EV。STC样细胞在AMA引起的TEC损伤中赋予的保护作用部分被其EV模仿。此外，STC样细胞-EV携带线粒体材料并将其转移至受损的TEC，从而部分恢复了线粒体功能。在体内，源自STC样细胞的EV植入了狭窄的肾脏，并改善了其灌注和氧合。STC样细胞-EV在体外和体内均对受损的肾小管细胞产生保护作用，部分是通过转移STC样细胞的线粒体而实现的，线粒体至少在受体TEC中保持部分功能。STC样细胞在AMA引起的TEC损伤中赋予的保护作用部分被其EV模仿。此外，STC样细胞-EV携带线粒体材料并将其转移至受损的TEC，从而部分恢复了线粒体功能。在体内，源自STC样细胞的EV植入了狭窄的肾脏，并改善了其灌注和氧合。STC样细胞-EV在体外和体内均对受损的肾小管细胞产生保护作用，部分是通过转移STC样细胞的线粒体而实现的，线粒体至少在受体TEC中保持部分功能。STC样细胞在AMA引起的TEC损伤中赋予的保护作用部分被其EV模仿。此外，STC样细胞-EV携带线粒体材料并将其转移到受损的TEC，从而部分恢复了线粒体功能。在体内，源自STC样细胞的EV植入了狭窄的肾脏，并改善了其灌注和氧合。STC样细胞-EV在体外和体内均对受损的肾小管细胞产生保护作用，部分是通过转移STC样细胞的线粒体而实现的，线粒体至少在受体TEC中保持部分功能。STC样细胞来源的EV植入狭窄的肾脏，并改善了其灌注和氧合。STC样细胞-EV在体外和体内均对受损的肾小管细胞产生保护作用，部分是通过转移STC样细胞的线粒体而实现的，线粒体至少在受体TEC中保持部分功能。STC样细胞来源的EV植入狭窄的肾脏，并改善了其灌注和氧合。STC样细胞-EV在体外和体内对受损的肾小管细胞发挥保护作用，部分是通过转移STC样细胞的线粒体来实现的，线粒体至少在受体TEC中保持部分功能。