Wang Liumin, Zhao Ying, Gang Shucheng, Geng Tongchao, Li Mingquan, Xu Lili, Zhang Xiaohao, Liu Ling, Xie Yi, Ye Ruidong, Liu Xinfeng
Department of Neurology, Taikang Xianlin Drum Tower Hospital, Medical School of Nanjing University, Nanjing, China.
Department of Neurology, Affiliated Jinling Hospital, Medical School of Nanjing University, Nanjing, China.
Neuroscience. 2021 May 1;461:91-101. doi: 10.1016/j.neuroscience.2021.03.007. Epub 2021 Mar 17.
Caveolin-1 (Cav-1) is a constitutive structural protein of caveolae in the plasma membrane. It plays an important role in maintaining blood brain barrier (BBB) integrity. In this study, we identified that miR-103-3p, a hypoxia-responsive miRNA, could interact with Cav-1. In endothelial cells, miR-103-3p mimic diminished the expression of Cav-1 and tight junction proteins, which were rescued by the inhibition of miR-103-3p. We found a substantial increase of miR-103-3p and decease of Cav-1 in the rat subarachnoid hemorrhage (SAH) model. Pre-SAH intracerebroventricularly injection of miR-103-3p antagomir relieved Cav-1 loss, sequentially reduced BBB permeability and improved neurological function. Finally, we demonstrated that the salutary effects of miR-103-3p antagomir were abolished in Cav-1 knock-out mice, suggesting that Cav-1 was required for the miR-103-3p inhibition-induced neurovascular protection. Taken together, our findings suggest that the inhibition of miR-103-3p could exert neuroprotective effects through preservation of Cav-1 and BBB integrity, making miR-103-3p a novel therapeutic target for SAH.
小窝蛋白-1(Cav-1)是质膜中小窝的一种组成性结构蛋白。它在维持血脑屏障(BBB)完整性方面发挥着重要作用。在本研究中,我们发现miR-103-3p,一种缺氧反应性微小RNA,可与Cav-1相互作用。在内皮细胞中,miR-103-3p模拟物降低了Cav-1和紧密连接蛋白的表达,而miR-103-3p的抑制可使其恢复。我们发现在大鼠蛛网膜下腔出血(SAH)模型中,miR-103-3p显著增加而Cav-1减少。SAH前脑室内注射miR-103-3p拮抗剂可减轻Cav-1的丢失,继而降低BBB通透性并改善神经功能。最后,我们证明在Cav-1基因敲除小鼠中,miR-103-3p拮抗剂的有益作用被消除,这表明Cav-1是miR-103-3p抑制诱导的神经血管保护所必需的。综上所述,我们的研究结果表明,抑制miR-103-3p可通过保留Cav-1和BBB完整性发挥神经保护作用,使miR-103-3p成为SAH的一个新的治疗靶点。