Du Jiang, Yang Qifen, Luo Lingfei, Yang Deqin
Key Laboratory of Freshwater Fish Reproduction and Development, Ministry of Education, Laboratory of Molecular Developmental Biology, School of Life Sciences, Southwest University, Beibei, 400715 Chongqing, China.
Key Laboratory of Freshwater Fish Reproduction and Development, Ministry of Education, Laboratory of Molecular Developmental Biology, School of Life Sciences, Southwest University, Beibei, 400715 Chongqing, China; Department of Endodontics and Operative Dentistry, Chongqing Key Laboratory for Oral Diseases and Biomedical Sciences, The Affiliated Hospital of Stomatology, Chongqing Medical University, 401147 Chongqing, China.
Biochem Biophys Res Commun. 2017 Jan 29;483(1):482-487. doi: 10.1016/j.bbrc.2016.12.118. Epub 2016 Dec 19.
Angiogenesis plays central role in the formation of functional circulation system. Characterizations of the involved factors and signaling pathways remain to be the key interest in the angiogenesis research. In this report, we showed that c1qr/cd93 and c1qrl/clec14a are specifically expressed in the vascular endothelial cells during zebrafish development. Single mutation of c1qr or c1qrl is associated with slightly malformation of inter-segmental vessels (ISVs), whereas double mutant exhibits severe defects in the ISVs formation without affecting early vasculogenesis. Further studies reveal that the endothelial-endothelial junctional molecule Cdh5 becomes absent in the ISVs of the double mutant. Replenishment of Cdh5 efficiently rescue the impaired angiogenesis in the c1qr/c1qrl double mutant. These data demonstrate that c1qr and c1qrl redundantly regulate angiogenesis through controlling the expression of the endothelial junctional molecule Cdh5, thus playing an important role in angiogenesis.
血管生成在功能性循环系统的形成中起着核心作用。对相关因子和信号通路的表征仍然是血管生成研究的关键兴趣点。在本报告中,我们表明c1qr/cd93和c1qrl/clec14a在斑马鱼发育过程中在血管内皮细胞中特异性表达。c1qr或c1qrl的单突变与节间血管(ISV)的轻微畸形有关,而双突变体在ISV形成中表现出严重缺陷,而不影响早期血管生成。进一步的研究表明,内皮-内皮连接分子Cdh5在双突变体的ISV中缺失。补充Cdh5可有效挽救c1qr/c1qrl双突变体中受损的血管生成。这些数据表明,c1qr和c1qrl通过控制内皮连接分子Cdh5的表达冗余调节血管生成,从而在血管生成中发挥重要作用。