Loss of JAM-C leads to impaired esophageal innervations and megaesophagus in mice
Loss of JAM-C leads to impaired esophageal innervations and megaesophagus in mice
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JAM-C 缺失会导致小鼠食管神经支配受损和巨食管
DOI：
10.1111/dote.12383
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发表时间：
2016-10-01
影响因子：
2.6
通讯作者：
Liang, X.
中科院分区：
文献类型：
--
作者：
Ye, M.;Zhang, Q.;Liang, X.
巨食管是一种疾病，其中没有适当地发生肿胀和食管扩大。巨食道症的病因和发病机制尚不清楚。在这项研究中，我们报道了C57/B6背景下的连接粘附分子C（JAM-C）敲除小鼠从胚胎第15.5天开始发展为进行性巨食管，并完全转移。JAM-C敲除小鼠表现出食管壁中神经纤维/神经节数量的显著减少。然而，组织学分析显示，JAM-C基因敲除小鼠在胚胎期和年轻成年时的食管壁厚度和结构与对照同窝小鼠相当。因此，在JAM-C基因敲除小鼠中观察到的巨食管症至少部分归因于食管神经支配受损。我们的数据表明，JAM-C作为一个潜在的候选基因的人巨食管，和JAM-C敲除小鼠可能作为一个模型，为人类巨食管的研究。
Megaesophagus is a disease where peristalsis fails to occur properly and esophagus is enlarged. The etiology and mechanism of megaesophagus are not well understood. In this study, we reported that junctional adhesion molecule C (JAM-C) knockout mice on a C57/B6 background developed progressive megaesophagus from embryonic day (E) 15.5 onward with complete penetrance. JAM-C knockout mice exhibited a significant reduction in the number of nerve fibers/ganglia in the wall of the esophagus. However, histological analysis revealed that the esophageal wall thickness and structure of JAM-C knockout mice at embryonic stages and young adult were comparable to that of control littermates. Thus, megaesophagus observed in JAM-C knockout mice could be attributed, at least in part, to impaired esophageal innervations. Our data suggest JAM-C as a potential candidate gene for human megaesophagus, and JAM-C knockout mice might serve as a model for the study of human megaesophagus.