Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14
pubmed:dateCreated
2005-12-1
pubmed:abstractText
The junctional adhesion molecule-C (JAM-C) was recently shown to be a counter receptor for the leukocyte beta2-integrin Mac-1 (CD11b/CD18), thereby mediating interactions between vascular cells, particularly in inflammatory cell recruitment. Here, we investigated the role of JAM-C in oxidized low-density lipoprotein (LDL)-mediated leukocyte recruitment. As compared with normal arteries, immunostaining of atherosclerotic vessels revealed a high expression of JAM-C in association with neointimal smooth muscle cells and the endothelium. Moreover, JAM-C was strongly up-regulated in the spontaneous early lesions in ApoE -/- mice. In vitro, cultured human arterial smooth muscle cells (HASMC) were found to express JAM-C, and oxLDL, as well as enzymatically modified LDL (eLDL) significantly up-regulated JAM-C on both HASMC and endothelial cells in a time- and dose-dependent manner. Although under quiescent conditions, JAM-C predominantly localized to interendothelial cell-cell contacts in close proximity to zonula occludens-1 (ZO-1), oxLDL treatment induced a disorganization of JAM-C localization that was no more restricted to the interendothelial junctions. JAM-C thereby mediated both leukocyte adhesion and leukocyte transendothelial migration upon oxLDL treatment of endothelial cells, whereas JAM-C on quiescent endothelial cells only mediates leukocyte transmigration. Thus, upon oxLDL stimulation endothelial JAM-C functions as both an adhesion, as well as a transmigration receptor for leukocytes. Taken together, JAM-C is up-regulated by oxLDL and may thereby contribute to increased inflammatory cell recruitment during atherosclerosis. JAM-C may therefore provide a novel molecular target for antagonizing interactions between vascular cells in atherosclerosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD11b, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD18, http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules, http://linkedlifedata.com/resource/pubmed/chemical/DNA, Complementary, http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G, http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulins, http://linkedlifedata.com/resource/pubmed/chemical/JAM3 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Lipoproteins, LDL, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Oxygen, http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1530-6860
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2078-80
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16195363-Aged, pubmed-meshheading:16195363-Animals, pubmed-meshheading:16195363-Antigens, CD11b, pubmed-meshheading:16195363-Antigens, CD18, pubmed-meshheading:16195363-Aorta, pubmed-meshheading:16195363-Atherosclerosis, pubmed-meshheading:16195363-Blotting, Western, pubmed-meshheading:16195363-Cell Adhesion, pubmed-meshheading:16195363-Cell Adhesion Molecules, pubmed-meshheading:16195363-Cell Movement, pubmed-meshheading:16195363-DNA, Complementary, pubmed-meshheading:16195363-Dose-Response Relationship, Drug, pubmed-meshheading:16195363-Endothelial Cells, pubmed-meshheading:16195363-Endothelium, Vascular, pubmed-meshheading:16195363-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:16195363-Female, pubmed-meshheading:16195363-Humans, pubmed-meshheading:16195363-Immunoglobulin G, pubmed-meshheading:16195363-Immunoglobulins, pubmed-meshheading:16195363-Immunohistochemistry, pubmed-meshheading:16195363-Inflammation, pubmed-meshheading:16195363-Leukocytes, pubmed-meshheading:16195363-Lipoproteins, LDL, pubmed-meshheading:16195363-Male, pubmed-meshheading:16195363-Membrane Proteins, pubmed-meshheading:16195363-Mice, pubmed-meshheading:16195363-Mice, Transgenic, pubmed-meshheading:16195363-Microscopy, Fluorescence, pubmed-meshheading:16195363-Middle Aged, pubmed-meshheading:16195363-Models, Biological, pubmed-meshheading:16195363-Monocytes, pubmed-meshheading:16195363-Muscle, Smooth, Vascular, pubmed-meshheading:16195363-Myocytes, Smooth Muscle, pubmed-meshheading:16195363-Oxygen, pubmed-meshheading:16195363-Recombinant Fusion Proteins, pubmed-meshheading:16195363-Recombinant Proteins, pubmed-meshheading:16195363-Time Factors, pubmed-meshheading:16195363-Umbilical Veins, pubmed-meshheading:16195363-Up-Regulation
pubmed:year
2005
pubmed:articleTitle
The role of junctional adhesion molecule-C (JAM-C) in oxidized LDL-mediated leukocyte recruitment.
pubmed:affiliation
Experimental Immunology Branch, NCI, NIH, Bethesda, Maryland 20892, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Intramural