Prostaglandins prevent decreased epithelial cell proliferation associated with dextran sodium sulfate injury in mice

T. G. Tessner, Steven Cohn, S. Schloemann, W. F. Stenson

Research output: Contribution to journalArticle

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Abstract

Background and Aims: Although dextran sodium sulfate (DSS)-induced colitis is a commonly used model of colonic injury, the mechanism of this model is not understood. The aim of this study was to determine the contribution of prostaglandins to the mechanism of DSS-induced epithelial injury. Methods: Mice were treated with 3% DSS in the drinking water for 5 days followed by water only (recovery). Tissue prostaglandin E2 (PGE2) levels were measured, proliferating cells per cecal crypt were determined by bromodeoxyuridine labeling, and the cellular localization of cyclooxygenase (COX)-1 and COX-2 was determined by immunohistochemistry. Results: DSS decreased the number of proliferating epithelial cells per crypt by approximately 90% and decreased the height of cecal crypts by 40%. Administration of dimethyl PGE2 with DSS reversed the effect of DSS on proliferation but not its effect on crypt shortening. COX-1 was expressed in the crypt epithelium and lamina propria mononuclear cells; DSS treatment down-regulated COX-1 expression only in the epithelium. Dimethyl PGE2 reversed the effect of DSS on COX-1 expression. Recovery was associated with a return to normal COX-1 expression in the epithelium. COX-2 was expressed in lamina propria mononuclear cells. Conclusions: Epithelial cell proliferation in the presence of DSS contains a PGE2-sensitive component.

Original languageEnglish (US)
Pages (from-to)874-882
Number of pages9
JournalGastroenterology
Volume115
Issue number4
DOIs
StatePublished - Jan 1 1998
Externally publishedYes

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Dextran Sulfate
Prostaglandins
Epithelial Cells
Cell Proliferation
Cyclooxygenase 1
Wounds and Injuries
Dinoprostone
Epithelium
Cyclooxygenase 2
Mucous Membrane
Bromodeoxyuridine
Colitis
Drinking Water
Immunohistochemistry
Water

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Prostaglandins prevent decreased epithelial cell proliferation associated with dextran sodium sulfate injury in mice. / Tessner, T. G.; Cohn, Steven; Schloemann, S.; Stenson, W. F.

In: Gastroenterology, Vol. 115, No. 4, 01.01.1998, p. 874-882.

Research output: Contribution to journalArticle

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abstract = "Background and Aims: Although dextran sodium sulfate (DSS)-induced colitis is a commonly used model of colonic injury, the mechanism of this model is not understood. The aim of this study was to determine the contribution of prostaglandins to the mechanism of DSS-induced epithelial injury. Methods: Mice were treated with 3{\%} DSS in the drinking water for 5 days followed by water only (recovery). Tissue prostaglandin E2 (PGE2) levels were measured, proliferating cells per cecal crypt were determined by bromodeoxyuridine labeling, and the cellular localization of cyclooxygenase (COX)-1 and COX-2 was determined by immunohistochemistry. Results: DSS decreased the number of proliferating epithelial cells per crypt by approximately 90{\%} and decreased the height of cecal crypts by 40{\%}. Administration of dimethyl PGE2 with DSS reversed the effect of DSS on proliferation but not its effect on crypt shortening. COX-1 was expressed in the crypt epithelium and lamina propria mononuclear cells; DSS treatment down-regulated COX-1 expression only in the epithelium. Dimethyl PGE2 reversed the effect of DSS on COX-1 expression. Recovery was associated with a return to normal COX-1 expression in the epithelium. COX-2 was expressed in lamina propria mononuclear cells. Conclusions: Epithelial cell proliferation in the presence of DSS contains a PGE2-sensitive component.",
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