Gastroenterology

Gastroenterology

Volume 109, Issue 1, July 1995, Pages 24-31
Gastroenterology

Up-regulation of transforming growth factor α binding sites in experimental rabbit colitis,☆☆

https://doi.org/10.1016/0016-5085(95)90265-1Get rights and content

Abstract

Background & Aims: Transforming growth factor α (TGF-α), a member of the epidermal growth factor family, has been proposed to mediate protection against mucosal injury and promote healing of the gastrointestinal mucosa. TGF-α acts via a plasma membrane receptor, which is distributed throughout the digestive system with the highest density in epithelia. The aim of this study was to investigate the pattern of TGF-α binding sites in the normal and inflamed rabbit colon. Methods: The immune complex/formalin model of acute colitis and tissue section receptor autoradiography were used. Inflammation was characterized by cellular infiltration, edema, and necrosis. TGF-α binding relative density was determined by densitometry on film autoradiograms. Results: The normal colon had a low to moderate density of specific TGF-α binding sites in the mucosa and external muscle. TGF-α binding density was significantly increased in the mucosa at 4 hours and remained higher than normal for up to 48 hours. The density of binding sites in the mucosa and the inflammatory index returned to near normal values at 96 hours, when colitis had subsided. Conclusions: The increase in TGF-α binding in the mucosa during experimental colitis supports the hypothesis that members of the epidermal growth factor family play a role in inflammation, perhaps acting as mediators of mucosal protection and repair.

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Supported by the Harbor-UCLA Inflammatory Bowel Disease Center, grant DK 41301 from the National Institutes of Health, CURE: VA/UCLA Gastroenteric Biology Center “Neuroendocrine Anatomy Core” subsection (to C.S.), Veterans Administration Medical Research Funds (to N.C.B.), and a fellowship from the “Ministero dell' Universitá della Ricerca Scientifica e Tecnologica” (to M.S.).

☆☆

Presented in part at the 1991 annual meeting of the American Gastroenterological Association and published in abstract form (Gastroenterology 1991; 100: A667).

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