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) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend 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 FOSTER, L. C. Articles by PERRELLA, M. A. Search for Related Content PubMed PubMed Citation Articles by FOSTER, L. C. Articles by PERRELLA, M. A.

Role of activating protein-1 and high mobility group-I(Y) protein in the induction of CD44 gene expression by interleukin-1ß in vascular smooth muscle cells

LAUREN C. FOSTER^*, PHILIPPE WIESEL^*,, GORDON S. HUGGINS^*,,¶, REA PAÑARES^*, MICHAEL T. CHIN^*,,, ANDREA PELLACANI^*,, and MARK A. PERRELLA^*,,§1

^* Cardiovascular Biology Laboratory, Harvard School of Public Health, Boston, Massachusetts 02115, USA;
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA;
Cardiovascular and
^§ Pulmonary and Critical Care Divisions, Brigham and Women’s Hospital, Boston, Massachusetts 02115, USA; and
^¶ Cardiac Unit, Massachusetts General Hospital, Boston, Massachusetts 02115, USA

¹Correspondence: Program of Developmental Cardiovascular Biology, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, USA. E-mail: perrella{at}cvlab.harvard.edu

CD44 is a multifunctional cell adhesion molecule that participates in pathological states such as inflammation and tumorigenesis. CD44 is induced on vascular smooth muscle cells after arterial wall injury and may mediate their proliferation and migration into the neointima during arteriosclerosis. We have demonstrated elsewhere that the proinflammatory cytokine interleukin (IL)-1ß up-regulates CD44 mRNA and protein expression in cultured rat aortic smooth muscle cells (RASMC) by increasing gene transcription. By transient transfection of 5'-deletion constructs into RASMC, we show in the present study that a conserved AP-1 site 110 base pairs from the transcription start site of the mouse CD44 promoter is important for basal activity. Mutation of the AP-1 site significantly reduced induction of promoter activity by IL-1ß, and electrophoretic mobility shift assays demonstrated that Fos and c-Jun were present in the CD44 AP-1 binding complex after IL-1ß stimulation. In addition, cotransfection of the architectural transcription factor high mobility group (HMG)-I(Y) protein with c-Fos and c-Jun markedly increased trans-activation of the CD44 promoter. Taken together, our studies demonstrate that AP-1 proteins are a central regulatory component used by IL-1ß to modulate expression of CD44 during an inflammatory response in vascular smooth muscle cells and that transcription of CD44 by AP-1 proteins is enhanced by HMG-I(Y).—Foster, L. C., Wiesel, P., Huggins, G. S, Pañares, R., Chin, M. T., Pellacani, A., Perrella, M. A. Role of activating protein-1 and high mobility group-I(Y) protein in the induction of CD44 gene expression by interleukin-1ß in vascular smooth muscle cells.

Key Words: inflammation • gene transcription • adhesion molecule • arteriosclerosis

This article has been cited by other articles:

				C. P. Matthews, A. M. Birkholz, A. R. Baker, C. M. Perella, G. R. Beck Jr., M. R. Young, and N. H. Colburn Dominant-Negative Activator Protein 1 (TAM67) Targets Cyclooxygenase-2 and Osteopontin under Conditions in which It Specifically Inhibits Tumorigenesis Cancer Res., March 15, 2007; 67(6): 2430 - 2438. [Abstract] [Full Text] [PDF]

				J. P. Mishra, S. Mishra, K. Gee, and A. Kumar Differential Involvement of Calmodulin-dependent Protein Kinase II-activated AP-1 and c-Jun N-terminal Kinase-activated EGR-1 Signaling Pathways in Tumor Necrosis Factor-{alpha} and Lipopolysaccharide-induced CD44 Expression in Human Monocytic Cells J. Biol. Chem., July 22, 2005; 280(29): 26825 - 26837. [Abstract] [Full Text] [PDF]

				R. M. Baron, I. M. Carvajal, X. Liu, R. O. Okabe, L. E. Fredenburgh, A. A. Macias, Y.-H. Chen, K. Ejima, M. D. Layne, and M. A. Perrella Reduction of Nitric Oxide Synthase 2 Expression by Distamycin A Improves Survival from Endotoxemia J. Immunol., September 15, 2004; 173(6): 4147 - 4153. [Abstract] [Full Text] [PDF]

				B. Beitzel and F. Bushman Construction and analysis of cells lacking the HMGA gene family Nucleic Acids Res., September 1, 2003; 31(17): 5025 - 5032. [Abstract] [Full Text] [PDF]

				M. E. Ramos-Nino, L. Scapoli, M. Martinelli, S. Land, and B. T. Mossman Microarray Analysis and RNA Silencing Link fra-1 to cd44 and c-met Expression in Mesothelioma Cancer Res., July 1, 2003; 63(13): 3539 - 3545. [Abstract] [Full Text] [PDF]

				I. Bouallaga, S. Teissier, M. Yaniv, and F. Thierry HMG-I(Y) and the CBP/p300 Coactivator Are Essential for Human Papillomavirus Type 18 Enhanceosome Transcriptional Activity Mol. Cell. Biol., April 1, 2003; 23(7): 2329 - 2340. [Abstract] [Full Text] [PDF]

				H. Wang, Y. Zhan, L. Xu, G. Z. Feuerstein, and X. Wang Use of Suppression Subtractive Hybridization for Differential Gene Expression in Stroke : Discovery of CD44 Gene Expression and Localization in Permanent Focal Stroke in Rats Stroke, April 1, 2001; 32(4): 1020 - 1027. [Abstract] [Full Text]

				M. Kume, K. Komori, T. Matsumoto, T. Onohara, K. Takeuchi, Y. Yonemitsu, and K. Sugimachi Administration of a Decoy Against the Activator Protein-1 Binding Site Suppresses Neointimal Thickening in Rabbit Balloon-Injured Arteries Circulation, March 12, 2002; 105(10): 1226 - 1232. [Abstract] [Full Text] [PDF]