Source:http://linkedlifedata.com/resource/pubmed/id/11129059
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
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| pubmed:dateCreated |
2000-12-20
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| pubmed:abstractText |
Inflammation and tissue trauma during the surgical procedure reduce the peritoneal fibrinolytic capacity. These conditions promote adhesion formation, and are associated with increased expression of transforming growth factor beta 1 (TGF-beta1). The objective of the present study was to investigate whether TGF-beta1 regulates the expression of fibrinolytic components in peritoneal mesothelial cells. Human peritoneal mesothelial cells (HPMC) were cultured and treated with various concentrations of human recombinant TGF-beta1 (0.1, 1.0 and 10 ng/mL) for 24 h. Levels of tissue- and urokinase plasminogen activator (t-PA and uPA), plasminogen activator inhibitor type-1 (PAI-1) and type-2 (PAI-2) mRNA and protein were assessed by quantitative reverse transcriptase polymerase chain reaction (Q-RT-PCR) and ELISA, respectively. HPMC expressed these components at the gene and protein level. TGF-beta1 downregulated, dose-dependently t-PA mRNA and protein to about 50% of control values (p = 0.0010), and doubled PAI-1 protein production (p = 0.0008) compared to untreated controls. Although uPA gene expression increased in cells exposed to TGF-beta1, the corresponding protein concentration in conditioned media did not. PAI-2 was not affected, either at the gene or protein level. In conclusion, the results indicate that fibrinolytic capacity of mesothelial cells is reduced by TGF-beta1, suggesting that peritoneal adhesion formation induced by TGF-beta1 may be mediated, in part, through reduction in fibrin degradation capacity at an early stage of peritoneal tissue repair.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/PLAUR protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Plasminogen Activator Inhibitor 1,
http://linkedlifedata.com/resource/pubmed/chemical/Plasminogen Activator Inhibitor 2,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Urokinase Plasminogen...,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tissue Plasminogen Activator,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Urokinase-Type Plasminogen Activator
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| pubmed:status |
MEDLINE
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| pubmed:month |
Oct
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| pubmed:issn |
0036-5513
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
60
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
439-47
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:11129059-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:11129059-Epithelial Cells,
pubmed-meshheading:11129059-Fibrinolysis,
pubmed-meshheading:11129059-Gene Expression Profiling,
pubmed-meshheading:11129059-Humans,
pubmed-meshheading:11129059-Peritoneal Cavity,
pubmed-meshheading:11129059-Plasminogen Activator Inhibitor 1,
pubmed-meshheading:11129059-Plasminogen Activator Inhibitor 2,
pubmed-meshheading:11129059-RNA, Messenger,
pubmed-meshheading:11129059-Receptors, Cell Surface,
pubmed-meshheading:11129059-Receptors, Urokinase Plasminogen Activator,
pubmed-meshheading:11129059-Recombinant Proteins,
pubmed-meshheading:11129059-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:11129059-Tissue Plasminogen Activator,
pubmed-meshheading:11129059-Transforming Growth Factor beta,
pubmed-meshheading:11129059-Urokinase-Type Plasminogen Activator
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| pubmed:year |
2000
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| pubmed:articleTitle |
Differential regulation of mesothelial cell fibrinolysis by transforming growth factor beta 1.
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| pubmed:affiliation |
Department of Surgery, Sahlgrenska University Hospital/Ostra, Göteborg University, Sweden.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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