Intercellular adhesion molecule‐1 in extravasation of normal mononuclear and leukaemia cells

Mustjoki, Satu; Alitalo, Riitta; Elonen, Erkki; Carpén, Olli; Gahmberg, Carl G.; Vaheri, Antti

doi:10.1046/j.1365-2141.2001.02793.x

Cited by 23 publications

(26 citation statements)

References 56 publications

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“…Antibodies or statins that inhibit ICAM-1 or its ligand might be promising. 14,38,39 Another approach is to inhibit the activation of CXC chemokines by using chemokine receptor antagonists that have been developed to inhibit chemokine responses. 40,41 It was also reported that acute respiratory distress syndrome caused by radiation was prevented by the use of anti-IL-8 antibody.…”

Section: Figurementioning

confidence: 99%

Retinoic acid syndrome in NOD/scid mice induced by injecting an acute promyelocytic leukemia cell line

et al. 2004

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All-trans retinoic acid (ATRA) induces complete remission in patients with acute promyelocytic leukemia (APL). However, ATRA sometimes causes retinoic acid syndrome (RAS) characterized by respiratory distress, pleural effusions, fever and weight gain. To investigate the pathophysiology of RAS, we generated an animal model by injecting an APL cell line, NB4, into immunodeficient mice. When NOD/scid mice were injected intravenously with fully differentiated NB4 cells (1 Â 10 7 ) and then given a daily administration of ATRA, three of 12 mice died of pulmonary edema within 14 days. Pathologically, dilated lung capillary vessels and alveolar effusions were observed. After the injection, NB4 cells were detected in the lung within 2 days and in the pleural effusion later on. The gene expression levels of CXC chemokines (MIP-2 and KC) and ICAM-1 were increased in the lung and heart by the ATRA administration. In immunohistochemical analyses, MIP-2 was clearly detected in alveolar macrophages of the lung in mice with RAS. Dexamethasone treatment prevented the development of RAS and decreased the CXC chemokine mRNA expression in the lung. These findings suggested that the activation of adhesion molecules for leukocytes and expression of CXC chemokines in the lung are closely involved in triggering RAS.

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Section: Figurementioning

confidence: 99%

Retinoic acid syndrome in NOD/scid mice induced by injecting an acute promyelocytic leukemia cell line

et al. 2004

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“…We specifically examined the viral regulation of ␤ 1 integrins, ␤ 2 integrins, intracellular adhesion molecule 1 (ICAM-1) (CD54), and ICAM-3 (CD50) due to their roles in the early events in transendothelial migration (30,36). Furthermore, we wanted to elucidate the signal transduction pathways responsible for the changes in HCMV-induced monocyte migration.…”

mentioning

confidence: 99%

“…ICAM-1 and ICAM-3 are highly glycosylated type I transmembrane proteins and consist structurally of five extracellular IgG-like domains, a transmembrane region, and a short cytoplasmic tail (12,26,47). ICAM-1 is expressed primarily on activated endothelial cells and leukocytes and binds to both CD11a/CD18 and CD11b/CD18 (18,36). ICAM-3 binds to CD11a/CD18, dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN), and CD11d/CD18 and is expressed primarily by monocytes, macrophages, T cells, and B cells (15,55).…”

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confidence: 99%

Roles of Phosphatidylinositol 3-Kinase and NF-κB in Human Cytomegalovirus-Mediated Monocyte Diapedesis and Adhesion: Strategy for Viral Persistence

Smith

Bivins-Smith

Tilley³

et al. 2007

J Virol

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Infected peripheral blood monocytes are proposed to play a key role in the hematogenous dissemination of human cytomegalovirus (HCMV) to tissues, a critical step in the establishment of HCMV persistence and the development of HCMV-associated diseases. We recently provided evidence for a unique strategy involved in viral dissemination: HCMV infection of primary human monocytes promotes their transendothelial migration and differentiation into proinflammatory macrophages permissive for the replication of the original input virus. To decipher the mechanism of hematogenous spread, we focused on the viral dysregulation of early cellular processes involved in transendothelial migration. Here, we present evidence that both phosphatidylinositol 3-kinase [PI(3)K] and NF-B activities were crucial for the HCMV induction of monocyte motility and firm adhesion to endothelial cells. We found that the ␤ 1 integrins, the ␤ 2 integrins, intracellular adhesion molecule 1 (ICAM-1), and ICAM-3 were upregulated following HCMV infection and that they played a key role in the firm adhesion of infected monocytes to the endothelium. The viral regulation of adhesion molecule expression is complex, with PI(3)K and NF-B affecting the expression of each adhesion molecule at different stages of the expression cascade. Our data demonstrate key roles for PI(3)K and NF-B signaling in the HCMV-induced cellular changes in monocytes and identify the biological rationale for the activation of these pathways in infected monocytes, which together suggest a mechanism for how HCMV promotes viral spread to and persistence within host organs.

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“…Cleaved forms of uPAR, lacking the uPA-binding domain, are widely expressed both in vivo and in vitro, e.g. on the surface of different cell lines (25)(26)(27)(28)(29), in normal and neoplastic thyroid tissues (26), in blast cells of patients with acute leukemia (30), in cystic fluids from benign and malignant ovarian tumors (31), in human foreskin microvascular endothelial cells (32), and in human xenograft tumors implanted in mice (29,33). In monocyte-like cells, Nterminal sequencing of the cleaved forms and uPAR cleavage inhibition by uPA-inactivating antibodies showed that uPA could be physiologically responsible for D1 removal by cleaving the receptor at two specific sites, between Arg 83 and Ala 84 and between Arg 89 and Ser 90 , in the D1-D2 linker region (34).…”

mentioning

confidence: 99%

The Cleavage of the Urokinase Receptor Regulates Its Multiple Functions

Montuori

Carriero

Salzano

et al. 2002

Journal of Biological Chemistry

124

157

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The urokinase-type plasminogen activator (uPA) is able to cleave its cell surface receptor (uPAR) anchored to the cell membrane through a glycophosphatidylinositol tail. The cleavage leads to the formation of cell surface truncated forms, devoid of the N-terminal domain 1 (D1) and unmasks or disrupts, depending on the cleavage site, a sequence in the D1-D2 linker region (residues 88 -92), which in the soluble form is a potent chemoattractant for monocyte-like cells. To investigate the possible role(s) of the cleaved forms of cell surface glycophosphatidylinositol-anchored uPAR, uPAR-negative human embrional kidney 293 cells were transfected with the cDNA of intact uPAR (uPAR-293) or with cDNAs corresponding to the truncated forms of uPAR exposing (D2D3-293) or lacking (D2D3wc-293) the peptide 88 -92 (P88 -92). Cell adhesion assays and co-immunoprecipitation experiments indicated that the removal of D1, independently of the presence of P88 -92, abolished the lateral interaction of uPAR with integrins and its capability to regulate integrin adhesive functions. The expression of intact uPAR induced also a moderate increase in 293 cell proliferation, which was accompanied by the activation of ERK. Also this effect was abolished by D1 removal, independently of the presence of P88 -92. The expression of intact and truncated uPARs regulated cell directional migration toward uPA, the specific uPAR ligand, and toward fMLP, a bacterial chemotactic peptide. In fact, the uPA-dependent cell migration required the expression of intact uPAR, including D1, whereas the fMLP-dependent cell migration required the expression of a P88 -92 containing uPAR and was independent of the presence of D1. Together these observations indicate that uPA-mediated uPAR cleavage and D1 removal, occurring on the cell surface of several cell types, can play a fundamental role in the regulation of multiple uPAR functions.

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Intercellular adhesion molecule‐1 in extravasation of normal mononuclear and leukaemia cells

Cited by 23 publications

References 56 publications

Retinoic acid syndrome in NOD/scid mice induced by injecting an acute promyelocytic leukemia cell line

Retinoic acid syndrome in NOD/scid mice induced by injecting an acute promyelocytic leukemia cell line

Roles of Phosphatidylinositol 3-Kinase and NF-κB in Human Cytomegalovirus-Mediated Monocyte Diapedesis and Adhesion: Strategy for Viral Persistence

The Cleavage of the Urokinase Receptor Regulates Its Multiple Functions

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