Ujigo Satoshi, Kamei Naosuke, Hadoush Hikmat, Fujioka Yuki, Miyaki Shigeru, Nakasa Tomoyuki, Tanaka Nobuhiro, Nakanishi Kazuyoshi, Eguchi Akiko, Sunagawa Toru, Ochi Mitsuo
*Department of Orthopaedic Surgery, Graduate School of Biomedical & Health Sciences, Hiroshima University, Hiroshima, Japan †Translational Research Medical Center, Hiroshima University Hospital, Hiroshima, Japan ‡Department of Analysis and Control of Upper Extremity Function, Graduate School of Biomedical & Health Sciences, Hiroshima University, Hiroshima, Japan; and §Department of Pediatric gastroenterology, University of California San Diego, CA.
Spine (Phila Pa 1976). 2014 Jun 15;39(14):1099-107. doi: 10.1097/BRS.0000000000000356.
Experimental animal study of treatment of spinal cord injury (SCI).
To investigate the therapeutic effects of administering microRNA-210 (miR-210) to promote angiogenesis in a mouse SCI model.
Despite many previous studies regarding SCI, there is no established treatment in clinical practice. miRNAs have attracted immense attention because of their crucial role in human disease, and they have been proposed as potential new therapeutic targets for SCI.
At specific times after administration, mice were analyzed by several methods to examine the distribution of miR-210, histological angiogenesis and neurogenesis, functional recovery from SCI, and the expression levels of target genes of miR-210.
After injection of miR-210 into the lesion of the injured spinal cord, expression of endogenous miR-210 increased until 6 days after injection. The administration of miR-210 promoted angiogenesis and astrogliosis, and improved functional recovery after SCI compared with the noninjected controls. Furthermore, the area made up of axons and myelin in the spinal cord tissues caudal to the injury site was larger in mice injected with miR-210 than those of the controls. Apoptotic cell death was lower in mice administered miR-210. After administration of miR-210, the expressions of protein-tyrosine phosphate 1B and ephrin-A3, both gene targets of miR-210, were downregulated at the protein level and protein-tyrosine phosphate 1B expression was also downregulated at the transcriptional level.
MiR-210 might contribute to spinal cord repair by promoting angiogenesis via the inhibition of protein-tyrosine phosphate 1B and ephrin-A3.
N/A.
脊髓损伤（SCI）治疗的实验性动物研究。
在小鼠SCI模型中研究给予微小RNA-210（miR-210）促进血管生成的治疗效果。
尽管此前有许多关于SCI的研究，但临床实践中尚无既定的治疗方法。微小RNA因其在人类疾病中的关键作用而备受关注，并已被提议作为SCI潜在的新治疗靶点。
在给药后的特定时间，通过多种方法对小鼠进行分析，以检测miR-210的分布、组织学血管生成和神经发生、SCI后的功能恢复以及miR-210靶基因的表达水平。
将miR-210注射到受损脊髓损伤部位后，内源性miR-210的表达在注射后6天内增加。与未注射的对照组相比，给予miR-210可促进血管生成和星形胶质细胞增生，并改善SCI后的功能恢复。此外，注射miR-210的小鼠损伤部位尾侧脊髓组织中由轴突和髓鞘组成的区域比对照组的大。给予miR-210的小鼠凋亡细胞死亡较少。给予miR-210后，miR-210的两个基因靶点蛋白酪氨酸磷酸酶1B和ephrin-A3的表达在蛋白水平下调，蛋白酪氨酸磷酸酶1B的表达在转录水平也下调。
MiR-210可能通过抑制蛋白酪氨酸磷酸酶1B和ephrin-A3促进血管生成，从而有助于脊髓修复。
无。
