HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 289/5/C1085    most recent 00185.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Zhu, Y.-Q. Articles by Tan, X.-D. Search for Related Content PubMed PubMed Citation Articles by Zhu, Y.-Q. Articles by Tan, X.-D.

RECEPTORS AND SIGNAL TRANSDUCTION

TFF3 modulates NF-B and a novel negative regulatory molecule of NF-B in intestinal epithelial cells via a mechanism distinct from TNF-

¹Molecular and Cellular Pathobiology Program, Children’s Memorial Research Center, Children’s Memorial Hospital, Chicago; and ²Departments of Pathology and Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, Illinois

Submitted 19 April 2005 ; accepted in final form 6 July 2005

Trefoil factor 3 (intestinal trefoil factor) is a cytoprotective factor in the gut. Herein we compared the effect of trefoil factor 3 with tumor necrosis factor- on 1) activation of NF-B in intestinal epithelial cells; 2) expression of Twist protein (a molecule essential for downregulation of nuclear factor-B activity in vivo); and 3) production of interleukin-8. We showed that Twist protein is constitutively expressed in intestinal epithelial cells. Tumor necrosis factor- induced persistent degradation of Twist protein in intestinal epithelial cells via a signaling pathway linked to proteasome, which was associated with prolonged activation of NF-B. In contrast to tumor necrosis factor, trefoil factor 3 triggered transient activation of NF-B and prolonged upregulation of Twist protein in intestinal epithelial cells via an ERK kinase-mediated pathway. Unlike tumor necrosis factor-, transient activation of NF-B by trefoil factor 3 is not associated with induction of IL-8 in cells. To examine the role of Twist protein in intestinal epithelial cells, we silenced the Twist expression by siRNA. Our data showed that trefoil factor 3 induced interleukin-8 production after silencing Twist in intestinal epithelial cells. Together, these observations indicated that 1) trefoil factor 3 triggers a diverse signal from tumor necrosis factor- on the activation of NF-B and its associated molecules in intestinal epithelial cells; and 2) trefoil factor 3-induced Twist protein plays an important role in the modulation of inflammatory cytokine production in intestinal epithelial cells.

trefoil factor 3; signal transduction

This article has been cited by other articles:

				K. E. Barrett A new twist on trefoils. Focus on "TFF3 modulates NF-{kappa}B and a novel regulatory molecule of NF-{kappa}B in intestinal epithelial cells via a mechanism distinct from TNF-{alpha}" Am J Physiol Cell Physiol, November 1, 2005; 289(5): C1069 - C1071. [Full Text] [PDF]