| First Author | Ye M | Year | 2016 |
| Journal | Dis Esophagus | Volume | 29 |
| Issue | 7 | Pages | 864-871 |
| PubMed ID | 26123848 | Mgi Jnum | J:278609 |
| Mgi Id | MGI:6359148 | Doi | 10.1111/dote.12383 |
| Citation | Ye M, et al. (2016) Loss of JAM-C leads to impaired esophageal innervations and megaesophagus in mice. Dis Esophagus 29(7):864-871 |
| abstractText | 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. |
