ArticleThe Journal of clinical investigation1998
Dexamethasone protection of rat intestinal epithelial cells against oxidant injury is mediated by induction of heat shock protein 72.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 68 citations in OpenAlex.
- The Multiple Roles of Heat Shock Proteins in the Development of Inflammatory Bowel Disease.Current molecular medicine · 2025Review
- Efficiency of a dexamethasone nanosuspension as an intratympanic injection for acute hearing loss.Drug delivery · 2022Article
- Production and characterization of avian crypt-villus enteroids and the effect of chemicals.BMC veterinary research · 2020Article
- Hsp72 protects against liver injury via attenuation of hepatocellular death, oxidative stress, and JNK signaling.Journal of hepatology · 2018Article
- How bacteria-induced apoptosis of intestinal epithelial cells contributes to mucosal inflammation.International journal of inflammation · 2010Article
- Stress granule formation mediates the inhibition of colonic Hsp70 translation by interferon-gamma and tumor necrosis factor-alpha.American journal of physiology. Gastrointestinal and liver physiology · 2010Article
- Inflammation-induced, 3'UTR-dependent translational inhibition of Hsp70 mRNA impairs intestinal homeostasis.American journal of physiology. Gastrointestinal and liver physiology · 2009Article
- Principles for characterizing the potential human health effects from exposure to nanomaterials: elements of a screening strategy.Particle and fibre toxicology · 2005Article
- Heat shock treatment protects osmotic stress-induced dysfunction of the blood-brain barrier through preservation of tight junction proteins.Cell stress & chaperones · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Although the therapeutic actions of glucocorticoids are largely attributed to their anti-inflammatory and immunosuppressive effects, they have been implicated in enhancing tissue and cellular protection. In this study, we demonstrate that dexamethasone significantly enhances viability of IEC-18 rat small intestinal cells against oxidant-induced stress in a dose-dependent fashion. This protective action is mediated by induction of hsp72, the major inducible heat shock protein in intestinal epithelial cells. Dexamethasone stimulates a time- and dose-dependent response in hsp72 protein expression that parallels its effects on cell viability. Furthermore, the induction of hsp72 is tissue dependent, as nonintestinal epithelioid HeLa cells show differential induction of hsp72 expression in response to the same dexamethasone treatment. Antisense hsp72 cDNA transfection of IEC-18 cells abolishes the dexamethasone-induced hsp72 response, without significantly affecting constitutive expression of its homologue, hsc73. Dexamethasone treatment also significantly induces hsp72 protein expression in rat intestinal mucosal cells in vivo. These data demonstrate that glucocorticoids protect intestinal epithelial cells against oxidant-induced stress by inducing hsp72.
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Registered trials
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.