ERK and p38 MAP kinase pathways are mediators of intestinal epithelial wound-induced signal transduction.

Publication/Presentation Date

4-17-1997

Abstract

Repair of gastrointestinal epithelial injury involves cell migration, proliferation, and specific gene expression. The pathways responsible for epithelial wound signal transduction are poorly understood. Mechanical wounding of IEC-6 cell monolayers resulted in rapid activation of the extracellular signal-regulated kinase (ERK) and p38 MAP kinase pathways, while c-Jun amino-terminal protein kinases were not significantly activated. Two minutes after wounding cells at the wound edge strongly expressed cytoplasmic phospho-ERK. By five minutes, immunostaining was concentrated within the nucleus. Consistent with activated MAP kinase signaling cascades (which phosphorylate transcription factors implicated in immediate-early gene induction), monolayer wounding resulted in greater than 30- and 8-fold increases in c-Fos and early growth response-1 mRNA by Northern blot analysis, peaking at 20 minutes. Only slight increases in c-Jun mRNA were detected. Thus, intestinal epithelial wound signal transduction is, at least in part, mediated by activation of ERK and p38 MAP kinase signaling cascades. ERK and p38 pathways may regulate pathophysiologically relevant genes in wound repair by the induction of transcription factors.

Volume

233

Issue

2

First Page

389

Last Page

394

ISSN

0006-291X

Disciplines

Diagnosis | Medicine and Health Sciences | Other Analytical, Diagnostic and Therapeutic Techniques and Equipment | Radiology

PubMedID

9144545

Department(s)

Department of Radiology and Diagnostic Medical Imaging

Document Type

Article

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