C1q 通过 LAIR1-HIF1α-VEGF 通路促进卒中后血管生成。
C1q contributes to post-stroke angiogenesis via LAIR1-HIF1α-VEGF pathway.
机构信息
Department of Emergency Medicine, Nanjing Drum Tower Hospital Affiliated to Nanjing University School of Medicine, Nanjing, 210008, P.R. China.
Department of Emergency Medicine, the First Affiliated Hospital of Shenzhen University, Health Science Center, the Second People’s Hospital of Shenzhen, Shenzhen, 518035, P.R. China
出版信息
Front Biosci (Landmark Ed). 2019 Mar 1;24(6):1050-1059. doi: 10.2741/4767.
Vascular remodeling is a critical event following a stroke. It is a well known fact that C1q is the first molecule in the complement classical pathway. However, its role in the neovascularization that ocurs after a stroke, remains unclear. In this study, we investigated the effects of C1q on post-stroke angiogeneis in pMCAO rats. We found that increased C1q levels in IBZ enhanced angiogenesis in rats with pMCAO. C1q promoted viability and angiogenic function of RBMECs and HBMECs. Upregualtion of VEGF expression and secretion by C1q was also observed in RBMECs, HBMECs and in IBZ in pMCAO rats. Furthermore, we demonstrated that C1q enhanced angiogenic function of RBMECs through its receptor, LAIR1. The results show that administration of C1q enhanced neovascularization and reduced brain edema after pMCAO in rats. On the basis of these findings, we suggest that C1q plays an important role in post-stroke angiogenesis at least through LAIR- HIF1α-VEGF axis. C1q shows promise as a potential therapeutic candidate for stroke treatment.
血管重构是中风后的一个关键事件。众所周知，C1q 是补体经典途径中的第一个分子。然而，其在中风后发生的新血管生成中的作用尚不清楚。在这项研究中，我们研究了 C1q 对 pMCAO 大鼠中风后血管生成的影响。我们发现，IBZ 中 C1q 水平的升高增强了 pMCAO 大鼠的血管生成。C1q 促进了 RBMECs 和 HBMECs 的活力和血管生成功能。在 pMCAO 大鼠的 RBMECs、HBMECs 和 IBZ 中也观察到 C1q 上调了 VEGF 的表达和分泌。此外，我们证明 C1q 通过其受体 LAIR1 增强了 RBMECs 的血管生成功能。结果表明，C1q 给药可增强 pMCAO 大鼠的新血管生成并减少脑水肿。基于这些发现，我们认为 C1q 通过 LAIR-HIF1α-VEGF 轴在中风后血管生成中发挥重要作用。C1q 有望成为中风治疗的潜在治疗候选物。
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