Cross-linking of Intercellular Adhesion Molecule-1 Induces Interleukin-8 and RANTES Production through the Activation of MAP Kinases in Human Vascular Endothelial Cells

Sano, Hideki; Nakagawa, Noriaki; Chiba, Ryuichi; Kurasawa, Kazuhiro; Saitō, Yasushi; Iwamoto, Itsuo

doi:10.1006/bbrc.1998.9385

Cited by 72 publications

(60 citation statements)

References 38 publications

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“…This induction was initiated as a result of the ICAM-1/␤ 2 integrin interaction and could be mimicked by crosslinking ICAM-1 with specific antibodies. Taken together with the observations that ICAM-1 cross-linking initiated the synthesis of vascular cell adhesion molecule-1 (26,27) and the chemokines IL-8 and RANTES (28), these observations suggest that cellular activation, through ICAM-1, may trigger a potent positive feedback mechanism for mediating the accumulation of leukocytes at sites of inflammation.…”

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confidence: 62%

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

Blaber¹,

Stylianou²,

Clayton³

et al. 2003

Journal of the American Society of Nephrology

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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 ␤ 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 [Ca 2ϩ ] i -dependent manner, with a maximum phosphorylation at approximately 3 min after crosslinking. 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-␣, which were not [Ca 2ϩ ] i -dependent. Electrophoretic mobility shift analysis demonstrated a time-dependent induction of both AP-1 and NF-B binding activity in nuclear extracts, maximal at approximately 15 min after ICAM-1 cross-linking. Only AP-1 activation, however, was calciumdependent, 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. steadmanr@cf.ac.uk An influx of leukocytes, particularly macrophages and lymphocytes, into the glomerulus and subsequently into the cortical interstitium is characteristic of most forms of progressive renal disease [see reference 1 for review and references 2-11). The initial interaction of the infiltrating cells is with the endothelial lining of the vessels. After migration through the endothelium, however, the principal interaction of leukocytes is with cortical fibroblasts, which, under inflammatory conditions, have the phenotypic appearance of myofibroblasts (8,(12)(13)(14)(15)(16). This interaction is mediated through the increased expression of intercellular adhesion molecule-1 (ICAM-1) (17-22) on the surface of the myofibroblasts and is central to the progression of inflammatory renal disease (2-11).ICAM-1 is a heavily glycosylated, single-chain transmembrane receptor induced by inflammatory cytokines at sites of inflammation, where it forms the counter-receptor for the leukocyte ␤ 2 integrins (23-25). We have recently demonstrated, for the first time, that leukocyte adherence to primary cultures of human renal fibroblasts was a stimulus for ICAM-1 induction (26). This induction was initiated as a result of the ICAM-1/␤ 2 integrin ...

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confidence: 62%

“…ERK 1 and 2, for example, were activated in human umbilical vein endothelial cells and in these cells this was directly related to the induction of IL-8 and RANTES (28). In contrast, there was no ERK activation detected following ICAM-1 cross-linking in endothelial cells isolated from the brain microvasculature (31).…”

Section: Discussionmentioning

confidence: 99%

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

Blaber¹,

Stylianou²,

Clayton³

et al. 2003

Journal of the American Society of Nephrology

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“…Tyrosine phosphorylation of MAP kinase is associated with LPS-induced TNF-␣ production in mice (13). RANTES mRNA expressions were induced through the activation of MAP kinases in endothelial cells (32), or through JNK and NF-B kinase cascades in macrophages stimulated with LPS (33). The Syk-generated signal cooperates to enhance Racinduced JNK activation in T lymphocytes (35), and MAP kinase activation was compromised in the macrophages of Syk Ϫ/Ϫ mice after Fc-␥ receptor stimulation (36).…”

Section: Discussionmentioning

confidence: 96%

Protein-Tyrosine Kinase Syk Expressed in Human Nasal Fibroblasts and Its Effect on RANTES Production

Yamada

Fujieda

Yanagi

et al. 2001

The Journal of Immunology

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Fibroblasts, a rich source of chemokines, interact with eosinophils and play a key role in the pathogenesis of airway disease. RANTES is produced by fibroblasts to attract and activate eosinophils. LPS is known to induce RANTES and cause protein tyrosine phosphorylation. Nonreceptor protein tyrosine kinase Syk is widely expressed and an important role in intracellular signal transduction in hemopoietic cells. In the present study, we examined whether Syk was expressed in a number of primary human nasal polyp tissue-derived fibroblast lines and whether it played some role in cellular function. Syk proteins were expressed in human nasal fibroblasts, but the expression level varied. There were positive correlations between the level of Syk expression and RANTES production induced by LPS. Overexpression of wild-type Syk by gene transfer enhanced RANTES production from nasal fibroblasts stimulated with LPS. The decrease of Syk expression by the administration of Syk antisense inhibited RANTES production. These results suggest that Syk expression affects RANTES production in fibroblasts of nasal polyps.

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“…MAPK-kinase pathways ERK-1/2 and/or JNK have been shown to the triggered depending on experimental design and cell type (Etienne, Adamson et al 1998;Sano, Nakagawa et al 1998;Lawson, Ainsworth et al 1999;Lawson, Ainsworth et al 2001). We have demonstrated that AP-1 activation is the result of ERK-1 activation (Lawson, Ainsworth et al 1999), together with the ERK-dependent production and secretion of IL-8 and RANTES (Sano, Nakagawa et al 1998) as well as upregulation of VCAM-1 on the cell surface (Lawson, Ainsworth et al 1999;Lawson, Ainsworth et al 2001).…”

Section: Signalling Via Icam-1mentioning

confidence: 99%

ICAM-1: Contribution to Vascular Inflammation and Early Atherosclerosis

Wolf¹

2012

Coronary Artery Disease - New Insights and Novel Approaches

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Cross-linking of Intercellular Adhesion Molecule-1 Induces Interleukin-8 and RANTES Production through the Activation of MAP Kinases in Human Vascular Endothelial Cells

Cited by 72 publications

References 38 publications

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

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

Protein-Tyrosine Kinase Syk Expressed in Human Nasal Fibroblasts and Its Effect on RANTES Production

ICAM-1: Contribution to Vascular Inflammation and Early Atherosclerosis

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