| pubmed-article:14675098 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14675098 | lifeskim:mentions | umls-concept:C0030190 | lld:lifeskim |
| pubmed-article:14675098 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:14675098 | lifeskim:mentions | umls-concept:C0483249 | lld:lifeskim |
| pubmed-article:14675098 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:14675098 | lifeskim:mentions | umls-concept:C0040044 | lld:lifeskim |
| pubmed-article:14675098 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:14675098 | pubmed:dateCreated | 2003-12-16 | lld:pubmed |
| pubmed-article:14675098 | pubmed:abstractText | Several activated coagulation factors have been reported to enhance fibrinolysis by neutralizing plasminogen activator inhibitor type 1 (PAI-1) activity. We evaluated the physiological relevance of this mechanism using the euglobulin clot lysis time (ECLT) assay in the presence and absence of Ca2+, which is controlled by PAI-1 and mimics physiological thrombolysis. We found that the ECLT (18.5 +/- 0.6 h) was shortened by Ca2+ (5 mm) (6.6 +/- 0.1 h). A significant difference was observed in thrombin generation by the presence of Ca2+ in the euglobulin fraction. Prothrombin was almost fully converted to thrombin within 15 min in the presence of Ca2+, whereas essentially no conversion was observed without Ca2+. The presence of activated protein C (aPC) suppressed thrombin generation, and attenuated the shortening of ECLT in a dose-dependent manner, an effect enhanced by phospholipid and protein S. In the absence of Ca2+, aPC did not prolong the ECLT. After addition of biotin-labeled recombinant PAI-1 to the euglobulin fraction, PAI-1 was cleaved to lower molecular weight forms only in the presence of Ca2+. This cleavage did not occur in the presence of aPC, suggesting that thrombin was the catalyst for PAI-1 cleavage. The cleavage and inactivation of PAI-1 by generated thrombin is proposed to be responsible for the shortening of ECLT by Ca2+ and for coagulation-associated over-expression of fibrinolysis. Under such conditions, aPC appeared to suppress thrombin generation and to normalize highly activated fibrinolysis. | lld:pubmed |
| pubmed-article:14675098 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14675098 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14675098 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14675098 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:14675098 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14675098 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:14675098 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14675098 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:14675098 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14675098 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14675098 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:14675098 | pubmed:issn | 1538-7933 | lld:pubmed |
| pubmed-article:14675098 | pubmed:author | pubmed-author:SuzukiYY | lld:pubmed |
| pubmed-article:14675098 | pubmed:author | pubmed-author:CastellinoF... | lld:pubmed |
| pubmed-article:14675098 | pubmed:author | pubmed-author:SuzukiKK | lld:pubmed |
| pubmed-article:14675098 | pubmed:author | pubmed-author:OhtaMM | lld:pubmed |
| pubmed-article:14675098 | pubmed:author | pubmed-author:MogamiHH | lld:pubmed |
| pubmed-article:14675098 | pubmed:author | pubmed-author:UranoTT | lld:pubmed |
| pubmed-article:14675098 | pubmed:author | pubmed-author:IharaHH | lld:pubmed |
| pubmed-article:14675098 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14675098 | pubmed:volume | 1 | lld:pubmed |
| pubmed-article:14675098 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14675098 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14675098 | pubmed:pagination | 2615-20 | lld:pubmed |
| pubmed-article:14675098 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:14675098 | pubmed:meshHeading | pubmed-meshheading:14675098... | lld:pubmed |
| pubmed-article:14675098 | pubmed:meshHeading | pubmed-meshheading:14675098... | lld:pubmed |
| pubmed-article:14675098 | pubmed:meshHeading | pubmed-meshheading:14675098... | lld:pubmed |
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| pubmed-article:14675098 | pubmed:meshHeading | pubmed-meshheading:14675098... | lld:pubmed |
| pubmed-article:14675098 | pubmed:meshHeading | pubmed-meshheading:14675098... | lld:pubmed |
| pubmed-article:14675098 | pubmed:meshHeading | pubmed-meshheading:14675098... | lld:pubmed |
| pubmed-article:14675098 | pubmed:meshHeading | pubmed-meshheading:14675098... | lld:pubmed |
| pubmed-article:14675098 | pubmed:meshHeading | pubmed-meshheading:14675098... | lld:pubmed |
| pubmed-article:14675098 | pubmed:meshHeading | pubmed-meshheading:14675098... | lld:pubmed |
| pubmed-article:14675098 | pubmed:meshHeading | pubmed-meshheading:14675098... | lld:pubmed |
| pubmed-article:14675098 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:14675098 | pubmed:articleTitle | Activated protein C attenuates coagulation-associated over-expression of fibrinolytic activity by suppressing the thrombin-dependent inactivation of PAI-1. | lld:pubmed |
| pubmed-article:14675098 | pubmed:affiliation | Department of Physiology, Hamamatsu University School of Medicine, Handa-yama, Hamamatsu, Japan. uranot@hama-med.ac.jp | lld:pubmed |
| pubmed-article:14675098 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:14675098 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:14675098 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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