Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2001-3-26
pubmed:abstractText
To assess the relationship between venous thrombosis and plasma glucosylceramide (GlcCer) or phosphatidylethanolamine (PE), plasma levels of GlcCer and PE were determined for 70 venous thrombosis patients referred for evaluation and 70 healthy blood donors. The mean GlcCer level, but not the PE level, was lower in patients versus controls (4.9 vs 6.5 microg/mL [P =.0007] and 66 vs 71 microg/mL [P =.48], respectively). As a measure of relative risk, the odds ratio for deep vein thrombosis in subjects with GlcCer levels below the 10th percentile of controls was 5.7 (95% CI, 2.3-14). To assess the influence of glycolipids on anticoagulant response to activated protein C (APC):protein S in modified prothrombin time assays, the effects of depleting endogenous plasma GlcCer by glucocerebrosidase treatment or of adding exogenous purified GlcCer or other neutral glycolipids to plasma were tested. Glucocerebrosidase treatment reduced plasma sensitivity to APC:protein S in parallel with GlcCer reduction. Exogenously added GlcCer and the homologous Glc-containing globotriaosylceramide (Gb3Cer), but not galactosylceramide, dose-dependently prolonged clotting times of normal plasma in the presence, but not absence, of APC:protein S, which suggests that GlcCer or Gb3Cer can enhance protein C pathway anticoagulant activity. In studies using purified proteins, inactivation of factor Va by APC:protein S was enhanced by GlcCer alone and by GlcCer in multicomponent vesicles containing phosphatidylserine and phosphatidylcholine. These results suggest that the neutral glycolipids GlcCer and Gb3Cer may directly contribute to the anticoagulant activity of the protein C pathway and that deficiency of plasma GlcCer may be a risk factor for venous thrombosis. (Blood. 2001;97:1907-1914)
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
97
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1907-14
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11264150-Activated Protein C Resistance, pubmed-meshheading:11264150-Adult, pubmed-meshheading:11264150-Aged, pubmed-meshheading:11264150-Aged, 80 and over, pubmed-meshheading:11264150-Blood Coagulation, pubmed-meshheading:11264150-Chromatography, High Pressure Liquid, pubmed-meshheading:11264150-Comorbidity, pubmed-meshheading:11264150-Contraceptives, Oral, Hormonal, pubmed-meshheading:11264150-European Continental Ancestry Group, pubmed-meshheading:11264150-Factor Va, pubmed-meshheading:11264150-Female, pubmed-meshheading:11264150-Galactosylceramides, pubmed-meshheading:11264150-Glucosylceramidase, pubmed-meshheading:11264150-Glucosylceramides, pubmed-meshheading:11264150-Humans, pubmed-meshheading:11264150-Male, pubmed-meshheading:11264150-Middle Aged, pubmed-meshheading:11264150-Neoplasms, pubmed-meshheading:11264150-Odds Ratio, pubmed-meshheading:11264150-Phosphatidylethanolamines, pubmed-meshheading:11264150-Postoperative Complications, pubmed-meshheading:11264150-Protein C, pubmed-meshheading:11264150-Protein S, pubmed-meshheading:11264150-Pulmonary Embolism, pubmed-meshheading:11264150-Risk, pubmed-meshheading:11264150-Thrombophilia, pubmed-meshheading:11264150-Trihexosylceramides, pubmed-meshheading:11264150-Venous Thrombosis, pubmed-meshheading:11264150-Wounds and Injuries
pubmed:year
2001
pubmed:articleTitle
Plasma glucosylceramide deficiency as potential risk factor for venous thrombosis and modulator of anticoagulant protein C pathway.
pubmed:affiliation
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't