Gadd45β promotes regeneration after injury through TGFβ-dependent restitution in experimental colitis

Cited 11 time in scopus
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Title
Gadd45β promotes regeneration after injury through TGFβ-dependent restitution in experimental colitis
Author(s)
Jung Hwan Hwang; T H Kim; Yong-Hoon KimJung-Ran NohDong Hee ChoiKyoung Shim KimEun-Young LeeByoung Chan KimMyung Hee Kim; H Kim; T G Lee; J S Lee; Chul Ho Lee
Bibliographic Citation
Experimental and Molecular Medicine, vol. 51, no. 10, pp. 128-128
Publication Year
2019
Abstract
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 (Gadd45β) has been implicated in the pathogenesis of various inflammatory symptoms. However, the role of Gadd45β in IBD is completely unknown. This study aimed to evaluate the role of Gadd45β in IBD. Gadd45β-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 Gadd45β functions predominantly in the intestinal epithelium and is critical during the recovery phase. Gadd45β regulates the TGF-β signaling pathway in colon tissue and epithelial cells by inhibiting Smurf-mediated degradation of TGF-β receptor type 1 via competitive binding to the N-terminal domain of Smad7. Furthermore, these results indicate that the Gadd45β-regulated TGF-β signaling pathway is involved in wound healing by enhancing epithelial restitution. These results expand the current understanding of the function of Gadd45β and its therapeutic potential in ulcerative colitis.
ISSN
I000-0028
Publisher
Springer-Nature Pub Group
DOI
http://dx.doi.org/10.1038/s12276-019-0335-y
Type
Article
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
Division of Biomedical Research > Microbiome Convergence Research Center > 1. Journal Articles
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