Role of leukocyte function-associated antigen-1 and very late antigen-4 in the adhesion and transmigration of c-myc-transfected B-lymphoblastoid cell lines across vascular endothelium

C. Paganin, G. Bianchi, L. Lombardi, R. Dalla Favera, A. Montovani, P. Allavena

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

The presented study was designed to characterize the adhesive interaction of c-myc-transfected B-lymphoblastoid cell lines with resting and interleukin-1-activated endothelial cells. The transfected cell lines expressed lower levels of leukocyte function-associated antigen-1 compared with control non-transfected lines, while no reduction of expression of other surface structures, including the β1 integrin very late antigen-4, was observed. The transfected cell lines adhered to resting or activated endothelial cells less than control cells. Anti-CD18 monoclonal antibody inhibited binding of control cell lines but had a modest or no effect on adhesion of transfected cell lines. Anti-very late antigen-4 monoclonal antibody effectively inhibited binding of both transfected and control cell lines; this was more pronounced in the presence of anti-CD18, suggesting a cooperative interaction between these adhesion pathways. Transfected cell lines also had an impaired ability to penetrate endothelial cell monolayers in a transmigration assay. Our results indicate that activation of the c-myc oncogene in B-cells causes alterations in the adhesive interaction with endothelial cells. This may be relevant in the localization and malignant behavior of B-cell lymphomas carrying an activated c-myc oncogene.

Original languageEnglish
Pages (from-to)29-32
Number of pages4
JournalInternational Journal of Clinical & Laboratory Research
Volume24
Issue number1
DOIs
Publication statusPublished - Jan 1994

Fingerprint

Integrin alpha4beta1
Lymphocyte Function-Associated Antigen-1
Vascular Endothelium
Adhesion
Cells
Cell Line
Endothelial cells
Endothelial Cells
myc Genes
Adhesives
Monoclonal Antibodies
B-Cell Lymphoma
Interleukin-1
Integrins
B-Lymphocytes
Surface structure
Monolayers
Assays
Chemical activation

Keywords

  • Adhesion
  • c-myc-Transfected B-lymphoblastoid cell lines
  • Endothelial cells
  • Leukocyte function-associated antigen-1
  • Very late antigen-4

ASJC Scopus subject areas

  • Clinical Biochemistry

Cite this

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title = "Role of leukocyte function-associated antigen-1 and very late antigen-4 in the adhesion and transmigration of c-myc-transfected B-lymphoblastoid cell lines across vascular endothelium",
abstract = "The presented study was designed to characterize the adhesive interaction of c-myc-transfected B-lymphoblastoid cell lines with resting and interleukin-1-activated endothelial cells. The transfected cell lines expressed lower levels of leukocyte function-associated antigen-1 compared with control non-transfected lines, while no reduction of expression of other surface structures, including the β1 integrin very late antigen-4, was observed. The transfected cell lines adhered to resting or activated endothelial cells less than control cells. Anti-CD18 monoclonal antibody inhibited binding of control cell lines but had a modest or no effect on adhesion of transfected cell lines. Anti-very late antigen-4 monoclonal antibody effectively inhibited binding of both transfected and control cell lines; this was more pronounced in the presence of anti-CD18, suggesting a cooperative interaction between these adhesion pathways. Transfected cell lines also had an impaired ability to penetrate endothelial cell monolayers in a transmigration assay. Our results indicate that activation of the c-myc oncogene in B-cells causes alterations in the adhesive interaction with endothelial cells. This may be relevant in the localization and malignant behavior of B-cell lymphomas carrying an activated c-myc oncogene.",
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AU - Paganin, C.

AU - Bianchi, G.

AU - Lombardi, L.

AU - Dalla Favera, R.

AU - Montovani, A.

AU - Allavena, P.

PY - 1994/1

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N2 - The presented study was designed to characterize the adhesive interaction of c-myc-transfected B-lymphoblastoid cell lines with resting and interleukin-1-activated endothelial cells. The transfected cell lines expressed lower levels of leukocyte function-associated antigen-1 compared with control non-transfected lines, while no reduction of expression of other surface structures, including the β1 integrin very late antigen-4, was observed. The transfected cell lines adhered to resting or activated endothelial cells less than control cells. Anti-CD18 monoclonal antibody inhibited binding of control cell lines but had a modest or no effect on adhesion of transfected cell lines. Anti-very late antigen-4 monoclonal antibody effectively inhibited binding of both transfected and control cell lines; this was more pronounced in the presence of anti-CD18, suggesting a cooperative interaction between these adhesion pathways. Transfected cell lines also had an impaired ability to penetrate endothelial cell monolayers in a transmigration assay. Our results indicate that activation of the c-myc oncogene in B-cells causes alterations in the adhesive interaction with endothelial cells. This may be relevant in the localization and malignant behavior of B-cell lymphomas carrying an activated c-myc oncogene.

AB - The presented study was designed to characterize the adhesive interaction of c-myc-transfected B-lymphoblastoid cell lines with resting and interleukin-1-activated endothelial cells. The transfected cell lines expressed lower levels of leukocyte function-associated antigen-1 compared with control non-transfected lines, while no reduction of expression of other surface structures, including the β1 integrin very late antigen-4, was observed. The transfected cell lines adhered to resting or activated endothelial cells less than control cells. Anti-CD18 monoclonal antibody inhibited binding of control cell lines but had a modest or no effect on adhesion of transfected cell lines. Anti-very late antigen-4 monoclonal antibody effectively inhibited binding of both transfected and control cell lines; this was more pronounced in the presence of anti-CD18, suggesting a cooperative interaction between these adhesion pathways. Transfected cell lines also had an impaired ability to penetrate endothelial cell monolayers in a transmigration assay. Our results indicate that activation of the c-myc oncogene in B-cells causes alterations in the adhesive interaction with endothelial cells. This may be relevant in the localization and malignant behavior of B-cell lymphomas carrying an activated c-myc oncogene.

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