Overexpressing dominant-negative FGFR2-IIIb impedes lung branching morphogenesis in pigs

查看全文 作　　者：Qin [1]Chen;Bin [1]Fang;Ying [1,2]Wang;Chu [1]Li;Xiaoxue [1]Li;Ronggen [1]Wang;Qiang [1]Xiong;Lining [1]Zhang;Yong [1]Jin;Manling [1,2]Zhang;Xiaorui [1]Liu;Lin [1,2]Li;Lisha [4]Mou;Rongfeng [1,2]Li;Haiyuan [1,2]Yang;Yifan [1,2,3,4]Dai

机构地区：[1]Jiangsu Key Laboratory of Xenotransplantation, Nanfing Medical University, Nanjing 211166, China;[2]Key Laboratory of Targeted intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine,Nanjing Medical University, Nanjing 211166, China;[3]State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing 211166, China;[4]Shenzhen Xenotransplantation Medical Engineering Research and Development Center, Institute of Translational Medicine, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, Shenzhen 518035, China

出　　处：《Journal of Genetics and Genomics》索引2018年第45卷第3期,共8页

基　　金：supported by grants from the National Natural Science Foundation of China(Nos.81570402 and 31701283);the National Key R&D Program of China(2017YFC1103701 and 2017YFC1103702);the Jiangsu Key Laboratory of Xenotransplantation(BM2012116);the Sanming Project of Medicine in Shenzhen(SZSM201412020);the Fund for High Level Medical Discipline Construction of Shenzhen(2016031638);the Shenzhen Foundation of Science and Technology(JCYJ20160229204849975 and GCZX2015043017281705) 摘　　要：Genetic studies with mouse models have shown that fibroblast growth factor receptor 2-IIIb(FGFR2-IIIb)plays crucial roles in lung development and differentiation. To evaluate the effect of FGFR2-IIIb in pig lung development, we employed somatic cell nuclear transfer(SCNT) technology to generate transgenic pig fetuses overexpressing the transmembrane(dn FGFR2-IIIb-Tm) and soluble(dn FGFR2-IIIb-HFc) forms of the dominant-negative human FGFR2-IIIb driven by the human surfactant protein C(SP-C) promoter,which was specifically expressed in lung epithelia. Eight dn FGFR2-IIIb-Tm transgenic and twelve dn FGFR2-IIIb-HFc transgenic pig fetuses were collected from three and two recipient sows, respectively.Repression of FGFR2-IIIb in lung epithelia resulted in smaller lobes and retardation of alveolarization in both forms of dn FGFR2-IIIb transgenic fetuses. Moreover, the dn FGFR2-IIIb-HFc transgenic ones showed more deterioration in lung development. Our results demonstrate that disruption of FGFR2-IIIb signaling in the epithelium impedes normal branching and alveolarization in pig lungs, which is less severe than the results observed in transgenic mice. The dn FGFR2-IIIb transgenic pig is a good model for the studies of blastocyst complementation as well as the mechanisms of lung development and organogenesis. 关键词：猪肺形态发生否定分叉转基因成纤维细胞表面活化剂生长因素

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Overexpressing dominant-negative FGFR2-IIIb impedes lung branching morphogenesis in pigs

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