IMR Press / FBL / Volume 24 / Issue 6 / DOI: 10.2741/4767

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
C1q contributes to post-stroke angiogenesis via LAIR1-HIF1α-VEGF pathway
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1 Department of Emergency Medicine, Nanjing Drum Tower Hospital Affiliated to Nanjing University School of Medicine, Nanjing, 210008, P.R. China
2 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
*Correspondence: jianqian08@gmail.com (Jian Qian)
Front. Biosci. (Landmark Ed) 2019, 24(6), 1050–1059; https://doi.org/10.2741/4767
Published: 1 March 2019
Abstract

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.

Keywords
C1q
Stroke
Angiogenesis
LAIR1
VEGF
HIF1 alpha
Figures
Figure 1.
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