Source:http://linkedlifedata.com/resource/pubmed/id/20823455
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
25
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pubmed:dateCreated |
2010-12-17
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pubmed:abstractText |
To explore the effect(s) of growth hormone signaling on thrombosis, we studied signal transduction and transcription factor 5 (STAT5)-deficient mice and found markedly reduced survival in an in vivo thrombosis model. These findings were not explained by a compensatory increase in growth hormone secretion. There was a modest increase in the activity of several procoagulant factors, but there was no difference in the rate or magnitude of thrombin generation in STAT5-deficient mice relative to control. However, thrombin-triggered clot times were markedly shorter, and fibrin polymerization occurred more rapidly in plasma from STAT5-deficient mice. Fibrinogen depletion and mixing studies indicated that the effect on fibrin polymerization was not due to intrinsic changes in fibrinogen, but resulted from changes in the concentration of a circulating plasma inhibitor. While thrombin-triggered clot times were significantly shorter in STAT5-deficient animals, reptilase-triggered clot times were unchanged. Accordingly, while the rate of thrombin-catalyzed release of fibrinopeptide A was similar, the release of fibrinopeptide B was accelerated in STAT5-deficient plasma versus control. Taken together, these studies demonstrated that the loss of STAT5 resulted in a decrease in the concentration of a plasma inhibitor affecting thrombin-triggered cleavage of fibrinopeptide B. This ultimately resulted in accelerated fibrin polymerization and greater thrombosis susceptibility in STAT5-deficient animals.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1528-0020
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
16
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pubmed:volume |
116
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5724-33
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pubmed:dateRevised |
2011-3-4
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pubmed:meshHeading |
pubmed-meshheading:20823455-Animals,
pubmed-meshheading:20823455-Blood Coagulation,
pubmed-meshheading:20823455-Disease Models, Animal,
pubmed-meshheading:20823455-Factor XIII,
pubmed-meshheading:20823455-Fibrin,
pubmed-meshheading:20823455-Fibrinopeptide B,
pubmed-meshheading:20823455-Immunoblotting,
pubmed-meshheading:20823455-Mice,
pubmed-meshheading:20823455-Mice, Inbred C57BL,
pubmed-meshheading:20823455-Mice, Knockout,
pubmed-meshheading:20823455-Pulmonary Embolism,
pubmed-meshheading:20823455-STAT5 Transcription Factor,
pubmed-meshheading:20823455-Signal Transduction,
pubmed-meshheading:20823455-Thrombin Time,
pubmed-meshheading:20823455-Thrombosis
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pubmed:year |
2010
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pubmed:articleTitle |
Increased thrombosis susceptibility and altered fibrin formation in STAT5-deficient mice.
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pubmed:affiliation |
Cardiovascular Research Institute, University of California, San Francisco, CA, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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