ArticleThe Journal of experimental medicine2013
Glucocorticoids alleviate intestinal ER stress by enhancing protein folding and degradation of misfolded proteins.
Article in The Journal of experimental medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 115 citations in OpenAlex.
- Myrrh ameliorates endometriosis by enhancing ER stress-related apoptotic cell death.Experimental and therapeutic medicine · 2026Article
- Krill oil supplementation alleviates clinical symptoms and improves intestinal barrier function with transcriptomic associations to cell adhesion molecule pathways in a mouse model of spontaneous chronic colitis.Frontiers in nutrition · 2026Article
- Mucin 2 and unfolded protein response reshape the mucus barrier in inflammatory bowel disease (Review).Molecular medicine reports · 2026Review
- 4-Phenylbutyric Acid Reduces the Proliferation in Colon Cancer Cell Lines Through Modulating the Cell Cycle Regulatory Genes: An In Silico and In Vitro Approach.Cancer reports (Hoboken, N.J.) · 2025Article
- Methylprednisolone Protects Human Pancreatic Beta Cells From Inflammation-induced Damage.Transplantation direct · 2025Article
- Winnie Mice: A Chronic and Progressive Model of Ulcerative Colitis.Inflammatory bowel diseases · 2025Review
- Chemogenomics for steroid hormone receptors (NR3).Communications chemistry · 2025Article
- Eicosanoids Signals in SARS-CoV-2 Infection: A Foe or Friend.Molecular biotechnology · 2024Review
- Review
- The IRE1α/XBP1 pathway sustains cytokine responses of group 3 innate lymphoid cells in inflammatory bowel disease.The Journal of clinical investigation · 2024Article
- The role of goblet cells in Crohn' s disease.Cell & bioscience · 2024Review
- Living, Heat-KilledNutrients · 2024Article
- Restore Intestinal Barrier Integrity: An Approach for Inflammatory Bowel Disease Therapy.Journal of inflammation research · 2024Review
- Prophylactic Prednisolone Promotes AAV5 Hepatocyte Transduction Through the Novel Mechanism of AAV5 Coreceptor Platelet-Derived Growth Factor Receptor Alpha Upregulation and Innate Immune Suppression.Human gene therapy · 2024Article
- RCN2 promotes Nasopharyngeal carcinoma progression by curbing Calcium flow and Mitochondrial apoptosis.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Protocadherin 20 maintains intestinal barrier function to protect against Crohn's disease by targeting ATF6.Genome biology · 2023Article
- Hyperglycemia-activated 11β-hydroxysteroid dehydrogenase type 1 increases endoplasmic reticulum stress and skin barrier dysfunction.Scientific reports · 2023Article
- Nanoparticles alleviate non-alcoholic steatohepatitis via ER stress sensor-mediated intestinal barrier damage and gut dysbiosis.Frontiers in microbiology · 2023Article
- IL-20 Activates ERK1/2 and Suppresses Splicing of X-Box Protein-1 in Intestinal Epithelial Cells but Does Not Improve Pathology in Acute or Chronic Models of Colitis.International journal of molecular sciences · 2022Article
- The role of goblet cells and mucus in intestinal homeostasis.Nature reviews. Gastroenterology & hepatology · 2022Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endoplasmic reticulum (ER) stress in intestinal secretory cells has been linked with colitis in mice and inflammatory bowel disease (IBD). Endogenous intestinal glucocorticoids are important for homeostasis and glucocorticoid drugs are efficacious in IBD. In Winnie mice with intestinal ER stress caused by misfolding of the Muc2 mucin, the glucocorticoid dexamethasone (DEX) suppressed ER stress and activation of the unfolded protein response (UPR), substantially restoring goblet cell Muc2 production. In mice lacking inflammation, a glucocorticoid receptor antagonist increased ER stress, and DEX suppressed ER stress induced by the N-glycosylation inhibitor, tunicamycin (Tm). In cultured human intestinal secretory cells, in a glucocorticoid receptor-dependent manner, DEX suppressed ER stress and UPR activation induced by blocking N-glycosylation, reducing ER Ca(2+) or depleting glucose. DEX up-regulated genes encoding chaperones and elements of ER-associated degradation (ERAD), including EDEM1. Silencing EDEM1 partially inhibited DEX's suppression of misfolding-induced ER stress, showing that DEX enhances ERAD. DEX inhibited Tm-induced MUC2 precursor accumulation, promoted production of mature mucin, and restored ER exit and secretion of Winnie mutant recombinant Muc2 domains, consistent with enhanced protein folding. In IBD, glucocorticoids are likely to ameliorate ER stress by promoting correct folding of secreted proteins and enhancing removal of misfolded proteins from the ER.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.