Department of Life Sciences, Faculty of Science and Engineering, Manchester Metropolitan University, Chester Street, Manchester, UK.
Department of Human Movement Sciences, Faculty of Behavioural and Movement Sciences, Vrije University Amsterdam, Amsterdam Movement Sciences, Amsterdam, The Netherlands.
Transl Stroke Res. 2021 Feb;12(1):125-135. doi: 10.1007/s12975-020-00805-0. Epub 2020 May 6.
Adipose-derived mesenchymal stem cells markedly attenuated brain infarct size and improved neurological function in rats. The mechanisms for neuronal cell death have previously been defined in stress states to suggest that an influx of calcium ions into the neurons activates calpain cleavage of p35 into p25 forming a hyperactive complex that induces cell death. Now we report that p5, a 24-residue peptide derived from p35, offers protection to neurons and endothelial cells in vitro. In vivo administration of human adipose-derived mesenchymal stem cells (hADMSCs) loaded with this therapeutic peptide to post-stroke rats had no effect on the infarct volume. Nevertheless, the treatment led to improvement in functional recovery in spatial learning and memory (water maze), bilateral coordination and sensorimotor function (rotating pole), and asymmetry of forelimb usage (cylinder test). However, the treatment may not impact on cutaneous sensitivity (adhesive tape removal test). In addition, the double immunofluorescence with human cell-specific antibodies revealed that the number of surviving transplanted cells was higher in the peri-infarcted area of animals treated with hADMSCs + P5 than that in hADMSC-treated or control animals, concomitant with reduced number of phagocytic, annexin3-positive cells in the peri-infarcted region. However, the combination therapy did not increase the vascular density in the peri-infarcted area after stroke. In conclusion, administration of hADMSC-loaded p5 peptide to post-stroke rats created conditions that supported survival of drug-loaded hADMSCs after cerebral ischemia, suggesting its therapeutic potential in patients with stroke.
脂肪间充质干细胞显著减轻了大鼠脑梗死体积并改善了神经功能。先前在应激状态下已定义了神经元细胞死亡的机制,表明钙离子流入神经元会激活钙蛋白酶将 p35 切割成 p25,形成超活性复合物,从而诱导细胞死亡。现在我们报告,源自 p35 的 24 个残基肽 p5 在体外对神经元和内皮细胞具有保护作用。将负载这种治疗性肽的人脂肪间充质干细胞 (hADMSC) 递送至中风后大鼠体内,对梗死体积没有影响。然而,该治疗导致空间学习和记忆(水迷宫)、双侧协调和感觉运动功能(旋转杆)以及前肢使用的不对称性(圆筒测试)的功能恢复得到改善。然而,该治疗可能不会影响皮肤敏感性(胶带去除测试)。此外,用人细胞特异性抗体的双重免疫荧光显示,在接受 hADMSC+P5 治疗的动物的梗死周围区域中,存活的移植细胞数量高于接受 hADMSC 治疗或对照动物的数量,同时在梗死周围区域中吞噬、膜联蛋白 3 阳性细胞的数量减少。然而,联合治疗并未增加中风后梗死周围区域的血管密度。总之,向中风后大鼠给予负载 p5 肽的 hADMSC 创造了条件,支持了脑缺血后载药 hADMSC 的存活,提示其在中风患者中的治疗潜力。