Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Front Med. 2021 Dec;15(6):887-902. doi: 10.1007/s11684-021-0879-9. Epub 2021 Dec 6.
Monocarboxylic acid transporter 1 (MCT1) maintains axonal function by transferring lactic acid from oligodendrocytes to axons. Subarachnoid hemorrhage (SAH) induces white matter injury, but the involvement of MCT1 is unclear. In this study, the SAH model of adult male Sprague-Dawley rats was used to explore the role of MCT1 in white matter injury after SAH. At 48 h after SAH, oligodendrocyte MCT1 was significantly reduced, and the exogenous overexpression of MCT1 significantly improved white matter integrity and long-term cognitive function. Motor training after SAH significantly increased the number of ITPR2SOX10 oligodendrocytes and upregulated the level of MCT1, which was positively correlated with the behavioral ability of rats. In addition, miR-29b and miR-124 levels were significantly increased in SAH rats compared with non-SAH rats. Further intervention experiments showed that miR-29b and miR-124 could negatively regulate the level of MCT1. This study confirmed that the loss of MCT1 may be one of the mechanisms of white matter damage after SAH and may be caused by the negative regulation of miR-29b and miR-124. MCT1 may be involved in the neurological improvement of rehabilitation training after SAH.
单羧酸转运蛋白 1（MCT1）通过将乳酸从少突胶质细胞转运到轴突来维持轴突功能。蛛网膜下腔出血（SAH）可引起白质损伤，但 MCT1 的参与尚不清楚。在这项研究中，使用成年雄性 Sprague-Dawley 大鼠的 SAH 模型来探讨 MCT1 在 SAH 后白质损伤中的作用。在 SAH 后 48 小时，少突胶质细胞 MCT1 明显减少，MCT1 的外源性过表达显著改善了白质完整性和长期认知功能。SAH 后进行运动训练显著增加了 ITPR2SOX10 少突胶质细胞的数量，并上调了 MCT1 的水平，这与大鼠的行为能力呈正相关。此外，与非 SAH 大鼠相比，SAH 大鼠中的 miR-29b 和 miR-124 水平明显升高。进一步的干预实验表明，miR-29b 和 miR-124 可以负调控 MCT1 的水平。这项研究证实，MCT1 的缺失可能是 SAH 后白质损伤的机制之一，可能是由 miR-29b 和 miR-124 的负调控引起的。MCT1 可能参与了 SAH 后康复训练引起的神经功能改善。
