Shabanzadeh Alireza P, Ringuette Dene, Syonov Michal, Wu Qisi, Tassew Nardos G, Mun Eric K, Meek Autumn, Lively Starlee, Suntharalingham Samuel E, Mojica Mia, Olijnyk Leonardo, Qiang Beiping, Foltz Warren D, Reed Mark, Moya Ignace, Brown Carla, Feng Jinzhou, Qin Xinyue, Akula Pavan Sudheer, Wälchli Thomas, Carlen Peter L, Alcaide-Leon Paula, Monnier Philippe P
Krembil Research Institute, University Health Network, Toronto, Ontario, Canada.
Krembil Brain Institute, University Health Network, Toronto, Ontario, Canada.
Nat Cardiovasc Res. 2025 Aug 26. doi: 10.1038/s44161-025-00691-5.
Neutralizing factors involved in blood vessel dysfunction offer a promising strategy for stroke recovery. Many extracellular proteins need enzymatic activation to function, and blocking this activation is an untapped approach to restoring vessel integrity. Here we demonstrate that inhibition of the extracellular protease SKI-1 with PF-429242 restores blood vessel integrity and promotes functional recovery in both large and small animal models for stroke. Single-cell mRNA sequencing identified molecular signatures suggesting that PF-429242 restores the expression of genes involved in vessel integrity in endothelial cells. Moreover, we identify a mechanism whereby RGMa cleavage by SKI-1 is required for RGMa to interact with Neogenin and alter vessel integrity. Either preventing RGMa cleavage or deleting Neogenin on endothelial cells reduced blood vessel dysfunction, increased tissue preservation and restored brain function after stroke. This work identifies a much-needed therapeutic strategy that restores blood vessel integrity and functionality, showing efficacy in large and small animals.
参与血管功能障碍的中和因子为中风恢复提供了一种有前景的策略。许多细胞外蛋白需要酶促激活才能发挥作用,而阻断这种激活是恢复血管完整性的一种尚未开发的方法。在这里,我们证明用PF-429242抑制细胞外蛋白酶SKI-1可恢复血管完整性,并促进大小动物中风模型的功能恢复。单细胞mRNA测序确定了分子特征,表明PF-429242可恢复内皮细胞中参与血管完整性的基因表达。此外,我们确定了一种机制,即SKI-1对RGMa的切割是RGMa与Neogenin相互作用并改变血管完整性所必需的。阻止RGMa切割或在内皮细胞上删除Neogenin均可减少血管功能障碍,增加组织保存并在中风后恢复脑功能。这项工作确定了一种急需的治疗策略,可恢复血管完整性和功能,在大小动物中均显示出疗效。