Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-5-7
pubmed:abstractText
Monocytes migrate through vascular endothelium, and then in connective tissue. As a model of this process, we investigated adhesion molecules involved in monocyte migration through HUVEC and a barrier of human synovial fibroblasts (HSF). Minimal spontaneous monocyte migration (6-7%) occurred through either cell barrier, but this increased markedly (27-35% of added monocytes) when a C5a chemotactic gradient was present. Migration across unstimulated HUVEC was partially inhibited (40%) by mAb to CD18 (beta2 integrin) and completely blocked by anti-CD18 plus anti-alpha4 (CD49d; very late Ag-4 (VLA-4)) mAbs. In contrast, migration across HSF induced by C5a or monocyte chemoattractant protein-1 was not inhibited by mAb to CD18 and was only partially inhibited (33%) in combination with anti-alpha4 mAb. The CD18- and VLA-4-independent migration across HSF was completely inhibited by mAb to alpha5 of VLA-5. The inhibitory effect of mAbs to VLA-4 and VLA-5 was on the monocyte and required blockade of CD11/CD18 to be observed. In contrast to HSF, no role for VLA-5 in monocyte transendothelial migration was detected. Both HSF and IL-1-stimulated HUVEC expressed vascular cell adhesion molecule-1 (VCAM-1). However, VLA-4-mediated monocyte migration across HSF was only partially dependent on VCAM-1, in contrast to transendothelial migration, which was completely blocked by anti-VCAM-1 mAbs. In conclusion, unlike transendothelial migration, for which VLA-4 is the alternative mechanism to CD11/CD18 on monocytes, both VLA-4 and VLA-5 can mediate monocyte migration through fibroblast barriers. In addition to VCAM-1, other ligand(s) on HSF are also involved in the VLA-4-mediated migration.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD11, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD18, http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules, http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2, http://linkedlifedata.com/resource/pubmed/chemical/Complement C5a, http://linkedlifedata.com/resource/pubmed/chemical/Integrin alpha4beta1, http://linkedlifedata.com/resource/pubmed/chemical/Integrin alpha6beta1, http://linkedlifedata.com/resource/pubmed/chemical/Integrins, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Fibronectin, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Lymphocyte Homing, http://linkedlifedata.com/resource/pubmed/chemical/Vascular Cell Adhesion Molecule-1
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
160
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
467-74
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9552005-Antibodies, Monoclonal, pubmed-meshheading:9552005-Antigens, CD11, pubmed-meshheading:9552005-Antigens, CD18, pubmed-meshheading:9552005-Cell Adhesion Molecules, pubmed-meshheading:9552005-Cell Movement, pubmed-meshheading:9552005-Chemokine CCL2, pubmed-meshheading:9552005-Complement C5a, pubmed-meshheading:9552005-Endothelium, pubmed-meshheading:9552005-Fibroblasts, pubmed-meshheading:9552005-Humans, pubmed-meshheading:9552005-Immunologic Techniques, pubmed-meshheading:9552005-Integrin alpha4beta1, pubmed-meshheading:9552005-Integrin alpha6beta1, pubmed-meshheading:9552005-Integrins, pubmed-meshheading:9552005-Monocytes, pubmed-meshheading:9552005-Receptors, Fibronectin, pubmed-meshheading:9552005-Receptors, Lymphocyte Homing, pubmed-meshheading:9552005-Synovial Membrane, pubmed-meshheading:9552005-Vascular Cell Adhesion Molecule-1
pubmed:year
1998
pubmed:articleTitle
Adhesion molecule mechanisms mediating monocyte migration through synovial fibroblast and endothelium barriers: role for CD11/CD18, very late antigen-4 (CD49d/CD29), very late antigen-5 (CD49e/CD29), and vascular cell adhesion molecule-1 (CD106).
pubmed:affiliation
Department of Pediatrics, Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't