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

Published online before print April 4, 2007

This Article Full Text Full Text (PDF) All Versions of this Article: jlb.1206754v1 82/2/213    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal 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 Google Scholar Google Scholar Articles by Hamilton, T. A. Articles by Li, X. Search for Related Content PubMed PubMed Citation Articles by Hamilton, T. A. Articles by Li, X.

(Journal of Leukocyte Biology. 2007;82:213-219.)
© 2007 by Society for Leukocyte Biology

Chemokine and chemoattractant receptor expression: post-transcriptional regulation

Department of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA

¹ Correspondence: Department of Immunology, NE40, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195, USA. E-mail: hamiltt{at}ccf.org

ABSTRACT

The magnitude and character of the inflammatory process are determined in part via the trafficking of leukocytes into sites of injury and infection, and this process depends on proper control of the expression of genes encoding chemoattractant peptides and their receptors. Although these controls operate at multiple mechanistic levels, recent evidence indicates that post-transcriptional events governing the half-life of select mRNAs are important determinants. Adenine-uridine rich elements (AREs) located within 3' untranslated regions (UTRs) confer constitutive mRNA instability and in some cases, stabilization following stimulation by ligands of the Toll-IL-1 receptor (TIR) family. Although the importance of AREs in determining activity and mRNA half-life is well-recognized, the mechanistic scope and diversity remain poorly understood. Using the mouse KC or CXCL1 gene as a model, we have demonstrated that the abundance of mRNA and protein produced during an inflammatory response depends on multiple mechanistically distinct AREs present in the 3' UTR of the mRNA. The mRNA encoding the receptor for N-terminal formyl-methionine-containing peptides is also unstable and subject to stabilization in response to TIR ligands. These two models can, however, be readily distinguished from one another on the basis of specific stimulus sensitivity and the signaling pathways, through which such stimuli couple to the control of mRNA decay. These models demonstrate the substantial diversity operative in the post-transcriptional regulation of inflammatory gene expression.

Key Words: mRNA stability • gene expression • inflammation

This article has been cited by other articles:

				C. L. Larson, D. H. Shah, A. S. Dhillon, D. R. Call, S. Ahn, G. J. Haldorson, C. Davitt, and M. E. Konkel Campylobacter jejuni invade chicken LMH cells inefficiently and stimulate differential expression of the chicken CXCLi1 and CXCLi2 cytokines Microbiology, December 1, 2008; 154(12): 3835 - 3847. [Abstract] [Full Text] [PDF]

				C. R. Stumpf, J. Kimble, and M. Wickens A Caenorhabditis elegans PUF protein family with distinct RNA binding specificity RNA, August 1, 2008; 14(8): 1550 - 1557. [Abstract] [Full Text] [PDF]

				J. H. Cox, R. A. Dean, C. R. Roberts, and C. M. Overall Matrix Metalloproteinase Processing of CXCL11/I-TAC Results in Loss of Chemoattractant Activity and Altered Glycosaminoglycan Binding J. Biol. Chem., July 11, 2008; 283(28): 19389 - 19399. [Abstract] [Full Text] [PDF]

				Q. Xu Stem Cells and Transplant Arteriosclerosis Circ. Res., May 9, 2008; 102(9): 1011 - 1024. [Abstract] [Full Text] [PDF]