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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1996-2-8
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pubmed:abstractText |
Other investigators have shown that exogenously administered transforming growth factor-beta (TGF-beta) inhibits lymphocyte adherence to vascular endothelial cells (VEC). We examined the role of TGF-beta 1 as an autocrine mediator of lymphocyte adhesion to adult human VECs. VECs were harvested from eight saphenous or cadaveric iliac veins using 0.2% collagenase. Low-passage VECs in MCDB + 0.1% BSA were pretreated for 24 hr with monoclonal anti-TGF-beta 1 antibody (5 micrograms/ml), LPS (5 micrograms/ml), or IL-1 (10 U/ml). Adherence of fluorescently labeled lymphocytes to pretreated VECs was quantitated and results were expressed as relative adhesion compared to untreated control. Total mRNA from LPS- or IL-1-treated VECs was subjected to Northern analysis to determine relative TGF-beta 1 expression. Total TGF-beta 1 protein concentration in supernatants from LPS- or IL-1-treated VECs was determined by ELISA. Data (means +/- SEM) were analyzed by ANOVA with a Newman-Keuls posttest. Neutralizing endogenous TGF-beta 1 with anti-TGF-beta 1 antibody significantly increased adhesion of lymphocytes to VEC monolayers compared to control (125 +/- 3 vs 101 +/- 2%, P < 0.01, n = 8). The level of adhesion was equivalent to that seen with IL-1 stimulation (131 +/- 6%). Spearman correlation of lymphocyte adherence to IL-1- or LPS-treated VECs vs TGF-beta 1 mRNA expression or vs relative TGF-beta 1 protein concentration showed significant inverse relationships (r = -0.82, P < 0.001, and r = -0.87, P < 0.001, respectively). Endogenous TGF-beta 1's inhibitory effect on lymphocyte adhesion was blocked by a specific neutralizing antibody. VEC TGF-beta 1 mRNA expression and TGF-beta 1 production were inversely proportional to lymphocyte adhesion, suggesting down-regulation of TGF-beta 1 in response to proinflammatory cytokines. Together, these observations support the hypothesis that TGF-beta 1 has an autocrine inhibitory role in regulation of lymphocyte adhesion to VECs.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0022-4804
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
59
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
719-24
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:8538171-Adult,
pubmed-meshheading:8538171-Blotting, Northern,
pubmed-meshheading:8538171-Cell Adhesion,
pubmed-meshheading:8538171-Cells, Cultured,
pubmed-meshheading:8538171-DNA,
pubmed-meshheading:8538171-Endothelium, Vascular,
pubmed-meshheading:8538171-Humans,
pubmed-meshheading:8538171-Lymphocytes,
pubmed-meshheading:8538171-RNA, Messenger,
pubmed-meshheading:8538171-Transforming Growth Factor beta
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pubmed:year |
1995
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pubmed:articleTitle |
Transforming growth factor-beta 1 serves as an autocrine inhibitor of human endothelial cell/lymphocyte adhesion.
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pubmed:affiliation |
Department of Surgery, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, Hershey 17033, USA.
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pubmed:publicationType |
Journal Article
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