Open AccessEndoplasmic Reticulum Stress in Subepithelial Myofibroblasts Increases the TGF-β1 Activity That Regulates Fibrosis in Crohn’s Disease
Author(s) -
Chao Li,
John R. Grider,
Karnam S. Murthy,
Jaime L. Bohl,
Emily B. Rivet,
Nicole Wieghard,
John F. Kuemmerle
Publication year - 2020
Publication title -
inflammatory bowel diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.932
H-Index - 146
eISSN - 1536-4844
pISSN - 1078-0998
DOI - 10.1093/ibd/izaa015
Subject(s) - endoplasmic reticulum , unfolded protein response , xbp1 , myofibroblast , crohn's disease , atf6 , transforming growth factor , transfection , tunicamycin , cancer research , fibrosis , gene knockdown , biology , microbiology and biotechnology , chemistry , endocrinology , medicine , apoptosis , biochemistry , rna splicing , disease , rna , gene
Endoplasmic reticulum (ER) stress is an essential response of epithelial and immune cells to inflammation in Crohn's disease. The presence and mechanisms that might regulate the ER stress response in subepithelial myofibroblasts (SEMFs) and its role in the development of fibrosis in patients with Crohn's disease have not been examined.