RT期刊文章SR电子T1神经生长因子增强肺损伤后的克拉拉细胞增殖摩根富林明欧洲呼吸杂志乔和J FD欧洲呼吸学会SP 105欧元OP 115做10.1183/09031936.00165508 VO 36是1 A1 S.S.声纳A1 d Schwinge A1。188bet官网地址科里奇A1同Yildirim A1马丁康拉德A1 K。赛德勒A1 b·穆勒A1 h .还建议A1西澳Nockher年2010 UL //www.qdcxjkg.com/content/36/1/105.abstract AB肺上皮细胞促进伤口关闭各种细胞因子和生长因子的分泌。神经生长因子(神经生长因子)气道炎症中描述;然而,它在肺修复中可能扮演的角色还没有检查。探讨修复神经生长因子的函数,实验使用培养的肺泡上皮细胞进行体外和体内使用naphthalene-induced克拉拉上皮细胞损伤模型。在体外和体内实验显示气道上皮细胞增殖后损伤是依赖于神经生长因子及其受体的表达,tropomyosin-receptor-kinase a .此外,神经生长因子也增强肺泡II型细胞的体外迁移。体内,转基因老鼠在克拉拉细胞过度表达神经生长因子(NGFtg)并没有透露任何增殖或克拉拉细胞表型的改变。然而,克拉拉细胞特定的伤害后,扩散增加NGFtg和受损的神经生长因子的抑制作用。 Furthermore, NGF also promoted the expression of collagen I and fibronectin in vitro and in vivo during repair, where significantly higher levels were measured in re-epithelialising NGFtg mice. Our study demonstrates that NGF promotes the proliferation of lung epithelium in vitro and the renewal of Clara cells following lung injury in vivo.