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- W165963399 abstract "Egr-1 is a key gene & transcription factor in experimental duodenal ulceration (Khomenko T et al. 2006). Role of Egr-1 in gastric ulcer (GU) pathogenesis is unclear. We tested the hypotheses that Egr-1 might play a role in the molecular mechanisms of experimental GU. GU was induced in male rats (150–190 g) by: immobilization (IMO) stress for 6, 12 & 24 hr; IMO stress combined with water-immersion (IMO-WI) for 20 min, 1 & 3 hr; ethanol (1 ml 96%, per os) for 20 min & 1 hr; aspirin (10 mg/100g, per os) for 20 min, 1 & 3 hr. Rats were euthanized immediately after ulcerogenic compound exposure. IMO-WI stress induced rapid early up-regulation of Egr-1 by 1.6- & 1.5-folds (p<0.05) at 20 min & 1 h and down-regulation - at 3 hr. IMO stress increased Egr-1 levels at 6 hr (2.1-folds, p<0.05) with gradual down-regulation by 24 hr. Ethanol & aspirin didn't change Egr-1 levels. IMO-WI stress but no aspirin & ethanol increased phosphorylation of Erk1/2 by 2.2; 2.6; 2.5-folds at 20 min, 1 & 3 hr (p<0.01), respectively & didn't change - p38. Erk2 was the major isoform expressed & phosphorylated. Conclusion Egr-1 plays a role in the early stages of stress-induced GU development vs. aspirin or ethanol; Erk1/2 might regulate Egr-1 activity during stress-induced GU." @default.
- W165963399 created "2016-06-24" @default.
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- W165963399 date "2013-04-01" @default.
- W165963399 modified "2023-09-27" @default.
- W165963399 title "TRANSCRIPTION FACTOR EGR‐1 IN MOLECULAR MECHANISMS OF EXPERIMENTAL GASTRIC ULCERS" @default.
- W165963399 doi "https://doi.org/10.1096/fasebj.27.1_supplement.1093.31" @default.
- W165963399 hasPublicationYear "2013" @default.
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