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Transcription Factors Regulating Embryonic Development of Pulmonary Vasculature

机译:调节肺脉管系统胚胎发育的转录因子

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Lung morphogenesis is a highly orchestrated process beginning with the appearance of lung buds on approximately embryonic day 9.5 in the mouse. Endodermally derived epithelial cells of the primitive lung buds undergo branching morphogenesis to generate the tree-like network of epithelial-lined tubules. The pulmonary vasculature develops in close proximity to epithelial progenitor cells in a process that is regulated by interactions between the developing epithelium and underlying mesenchyme. Studies in transgenic and knockout mouse models demonstrate that normal lung morphogenesis requires coordinated interactions between cells lining the tubules, which end in peripheral saccules, juxtaposed to an extensive network of capillaries. Multiple growth factors, microRNAs, transcription factors, and their associated signaling cascades regulate cellular proliferation, migration, survival, and differentiation during formation of the peripheral lung. Dysregulation of signaling events caused by gene mutations, teratogens, or premature birth causes severe congenital and acquired lung diseases in which normal alveolar architecture and the pulmonary capillary network are disrupted. Herein, we review scientific progress regarding signaling and transcriptional mechanisms regulating the development of pulmonary vasculature during lung morphogenesis.
机译:肺部形态发生是一种高度衡心的过程,从小鼠近似胚胎第9.5天的肺芽外观开始。原始肺芽的内固结衍生的上皮细胞经历了分支的形态发生,以产生类似的上皮衬里小管的树状网络。肺脉管系统在通过显影上皮和下面的间充质之间的相互作用调节的过程中,在上皮祖细胞附近发展。转基因和敲除小鼠模型的研究表明,正常的肺部形态发生需要在小管中衬里的细胞之间的协调相互作用,该小管在外围囊状中结束,并置于毛细血管广泛的网络中。多种生长因子,微大研讨会,转录因子及其相关的信号级联调节细胞增殖,迁移,生存和分化期间的外周肺。失去由基因突变,畸齿或过早出生引起的信号传导事件导致严重的先天性和获得的肺部疾病,其中正常的肺泡结构和肺毛细管网络被破坏。在此,我们审查了关于调节肺部形态发生期间肺脉管系统发育的信号传导和转录机制的科学进步。

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