Litingtung Y, Lei L, Westphal H, Chiang C
Department of Cell Biology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-2175, USA.
Nat Genet. 1998 Sep;20(1):58-61. doi: 10.1038/1717.
Congenital malformation of the foregut is common in humans, with an estimated incidence of 1 in 3000 live births, although its aetiology remains largely unknown. Mice with a targeted deletion of Sonic hedgehog (Shh) have foregut defects that are apparent as early as embryonic day 9.5, when the tracheal diverticulum begins to outgrow. Homozygous Shh-null mutant mice show oesophageal atresia/stenosis, tracheo-oesophageal fistula and tracheal and lung anomalies, features similar to those observed in humans with foregut defects. The lung mesenchyme shows enhanced cell death, decreased cell proliferation and downregulation of Shh target genes. These results indicate that Shh is required for the growth and differentiation of the oesophagus, trachea and lung, and suggest that mutations in SHH and its signalling components may be involved in foregut defects in humans.
前肠先天性畸形在人类中很常见,估计活产儿中的发病率为1/3000,但其病因在很大程度上仍不清楚。靶向敲除音猬因子(Shh)的小鼠在前肠出现缺陷,早在胚胎第9.5天就很明显,此时气管憩室开始向外生长。纯合子Shh基因敲除突变小鼠表现出食管闭锁/狭窄、气管食管瘘以及气管和肺部异常,这些特征与在前肠缺陷的人类中观察到的相似。肺间充质显示细胞死亡增加、细胞增殖减少以及Shh靶基因下调。这些结果表明,Shh是食管、气管和肺生长及分化所必需的,并提示SHH及其信号传导成分的突变可能与人类前肠缺陷有关。