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J Am Soc Nephrol 14:116-127, 2003
© 2003 American Society of Nephrology

Selective Regulation of ICAM-1 and RANTES Gene Expression after ICAM-1 Ligation on Human Renal Fibroblasts

Robert Blaber*, Eleni Stylianou{dagger}, Aled Clayton{dagger} and Robert Steadman*

*Institute of Nephrology, University of Wales College of Medicine, Heath Park, Cardiff, Wales, UK; {dagger}School of Biomedical Sciences, University Hospital, Queen’s Medical Centre, Nottingham, UK; {ddagger}Section of Clinical Oncology, Department of Medicine, University of Wales College of Medicine, Velindre Hospital, Cardiff, Wales, UK.

Correspondence to Dr. Robert Steadman, Institute of Nephrology, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, Wales. Phone: 44-0-29-2074-8390; Fax: 44-0-29-2074-8470.

ABSTRACT. Leukocyte infiltration of the cortico-interstitium is characteristic of many forms of progressive renal disease. The principal adhesion molecule expressed on resident interstitial cells and recognized by leukocytes is intercellular adhesion molecule–1 (ICAM-1). ICAM-1 is an inducible transmembrane receptor, which forms the counter-receptor for the leukocyte {beta}2 integrins. ICAM-1–dependent binding induces the synthesis of the chemokine RANTES and of ICAM-1 itself. This study examines some of the signaling pathways involved in this induction. After ICAM-1 cross-linking on fibroblasts, the mRNA and protein for both RANTES and ICAM-1 were induced. This induction was calcium-dependent and inhibited by BAPTA-AM. The p38, ERK1, and ERK2 MAP kinases were activated in a [Ca2+]i-dependent manner, with a maximum phosphorylation at approximately 3 min after cross-linking. Through the use of selective inhibitors of p38 MAP kinase (SB203580) or MEKK (PD98059), p38 but not ERK activation was shown to be essential for the induction of ICAM-1. Neither was involved in RANTES activation, however. These mechanisms differed from those initiated by TNF-{alpha}, which were not [Ca2+]i-dependent. Electrophoretic mobility shift analysis demonstrated a time-dependent induction of both AP-1 and NF-{kappa}B binding activity in nuclear extracts, maximal at approximately 15 min after ICAM-1 cross-linking. Only AP-1 activation, however, was calcium-dependent, suggesting the central involvement of this transcription factor in ICAM-1 and RANTES induction after the ligation of ICAM-1. This study suggests an independent mechanism of inflammatory amplification, which may be characteristic of a persistent leukocytic involvement in areas of chronic inflammation rather than in cytokine-induced acute inflammation. E-mail: Steadmanr@cf.ac.uk




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