| First Author | Hwang JH | Year | 2019 |
| Journal | Exp Mol Med | Volume | 51 |
| Issue | 10 | Pages | 1-14 |
| PubMed ID | 31666502 | Mgi Jnum | J:293615 |
| Mgi Id | MGI:6451276 | Doi | 10.1038/s12276-019-0335-y |
| Citation | Hwang JH, et al. (2019) Gadd45beta promotes regeneration after injury through TGFbeta-dependent restitution in experimental colitis. Exp Mol Med 51(10):1-14 |
| abstractText | Dysregulated immune responses and impaired function in intestinal epithelial cells contribute to the pathogenesis of inflammatory bowel disease (IBD). Growth arrest and DNA damage-inducible 45 beta (Gadd45beta) has been implicated in the pathogenesis of various inflammatory symptoms. However, the role of Gadd45beta in IBD is completely unknown. This study aimed to evaluate the role of Gadd45beta in IBD. Gadd45beta-KO mice exhibited drastically greater susceptibility to dextran sulfate sodium (DSS)-induced colitis and mortality than C57BL/6J mice. Bone marrow transplantation experiments revealed that Gadd45beta functions predominantly in the intestinal epithelium and is critical during the recovery phase. Gadd45beta regulates the TGF-beta signaling pathway in colon tissue and epithelial cells by inhibiting Smurf-mediated degradation of TGF-beta receptor type 1 via competitive binding to the N-terminal domain of Smad7. Furthermore, these results indicate that the Gadd45beta-regulated TGF-beta signaling pathway is involved in wound healing by enhancing epithelial restitution. These results expand the current understanding of the function of Gadd45beta and its therapeutic potential in ulcerative colitis. |
