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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
1995-11-22
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pubmed:abstractText |
Scarring, fibrosis, and immunosuppression occurs with chronic cyclosporine (CsA) administration. We postulated that CsA may induce transforming growth factor (TGF)-beta 1 secretion from human T lymphocytes, a cytokine with immunoregulatory effects that has been implicated in the pathogenesis of wound healing and scarring. TGF-beta 1 was measured in serum-free supernatants harvested from T lymphocytes stimulated in the presence of CsA by a specific sandwich ELISA. CsA (10-1000 ng/ml) enhanced TGF-beta 1 secretion by approximately 40-80% in a dose-dependent manner. Increased TGF-beta 1 secretion in the presence of CsA was accompanied by a 2- to 4-fold increase in TGF-beta 1 mRNA levels due to both enhancement of its nuclear transcription as well as prolongation of TGF-beta 1 mRNA half-life. To determine whether the increase in TGF-beta 1 secretion was also accompanied by a concomitant change in its receptor, TGF-beta 1 receptor expression was analyzed by cross-linking of radioiodinated TGF-beta 1. Unactivated T lymphocytes expressed both a 105-kDa and a 65-kDa TGF-beta receptor. Upon stimulation, a transient increase in receptor density was seen at 12 hr, followed by a decline at later time points. Cells treated with CsA exhibited at least 2-fold higher levels of TGF-beta receptors in a dose-dependent manner. Thus, CsA enhances the production of TGF-beta 1 protein as well as the expression of its receptor in activated T lymphocytes. Enhanced TGF-beta 1 production and binding may contribute to the immunosuppressive and fibrosis-promoting effects of CsA therapy.
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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/Cyclosporine,
http://linkedlifedata.com/resource/pubmed/chemical/Immunosuppressive Agents,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Transforming Growth...,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0041-1337
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
60
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
718-23
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:7570983-Adult,
pubmed-meshheading:7570983-Cyclosporine,
pubmed-meshheading:7570983-Humans,
pubmed-meshheading:7570983-Immunosuppressive Agents,
pubmed-meshheading:7570983-Lymphocyte Activation,
pubmed-meshheading:7570983-RNA, Messenger,
pubmed-meshheading:7570983-Receptors, Transforming Growth Factor beta,
pubmed-meshheading:7570983-T-Lymphocytes,
pubmed-meshheading:7570983-Time Factors,
pubmed-meshheading:7570983-Transcription, Genetic,
pubmed-meshheading:7570983-Transforming Growth Factor beta,
pubmed-meshheading:7570983-Up-Regulation
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pubmed:year |
1995
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pubmed:articleTitle |
Regulation of transforming growth factor-beta 1 and its receptor by cyclosporine in human T lymphocytes.
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pubmed:affiliation |
Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
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pubmed:publicationType |
Journal Article
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