AJP - GI Watch the video to learn how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Gastrointest Liver Physiol 295: G374-G381, 2008. First published June 26, 2008; doi:10.1152/ajpgi.90325.2008
0193-1857/08 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
295/2/G374    most recent
ajpgi.90325.2008v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dudar, G. K.
Right arrow Articles by Wallace, J. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dudar, G. K.
Right arrow Articles by Wallace, J. L.

MUCOSAL BIOLOGY

A vascular endothelial growth factor mimetic accelerates gastric ulcer healing in an iNOS-dependent manner

Genevieve K. Dudar,1 Luca D. D'Andrea,2 Rossella Di Stasi,2 Carlo Pedone,2 and John L. Wallace1

1Inflammation Research Network, University of Calgary, Calgary, Alberta, Canada; and 2Istituto di Biostrutture e Bioimmagini, Consiglio Nazionale delle Ricerche, Napoli, Italy

Submitted 5 May 2008 ; accepted in final form 20 June 2008

Angiogenesis is crucial to all types of wound healing, including gastric ulcer healing. The most potent promoter of angiogenesis is vascular endothelial growth factor (VEGF). We hypothesized that a 15-amino acid peptide designed to mimic the angiogenic action of VEGF would accelerate gastric ulcer healing. Gastric ulcers were induced in mice by serosal application of acetic acid. Treatment with the VEGF mimetic accelerated gastric ulcer healing when administered orally or intraperitoneally, at a dose of 50 ng/kg or greater. Such healing was not observed when the reverse sequence pentadecapeptide or the full-length VEGF protein was administered. Contrary to our hypothesis, the VEGF mimetic did not significantly increase angiogenesis in the ulcerated stomach. The enhancement of ulcer healing by the VEGF mimetic occurred independently of cyclooxygenase-2 (COX-2) activity but was blocked by inhibitors of inducible nitric oxide synthase (iNOS). These results demonstrate that a VEGF mimetic is a potent stimulus for gastric ulcer healing, even when given orally. The effects of the mimetic were independent of stimulatory effects on angiogenesis and COX-2 activity but were dependent on iNOS-derived NO production.

stomach; nitric oxide; cyclooxygenase; angiogenesis; prostaglandin; gastric mucosa


Address for reprint requests and other correspondence: J. Wallace, Dept. of Pharmacology & Therapeutics, Univ. of Calgary, 3330 Hospital Dr. NW, Calgary, Alberta, T2N 4N1, Canada (e-mail: wallacej{at}ucalgary.ca)






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.