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dc.contributor.authorKundur, Avinashen_US
dc.contributor.authorSanthakumar, Abisheken_US
dc.contributor.authorBulmer, Andrewen_US
dc.contributor.authorSingh, Induen_US
dc.date.accessioned2019-01-04T12:30:45Z
dc.date.available2019-01-04T12:30:45Z
dc.date.issued2017en_US
dc.identifier.issn0953-7104en_US
dc.identifier.doi10.1080/09537104.2017.1280146en_US
dc.identifier.urihttp://hdl.handle.net/10072/345138
dc.description.abstractGilbert’s syndrome (GS) is associated with a mild unconjugated hyperbilirubinemia, increased circulating antioxidant capacity, and reduced cardiovascular disease (CVD) risk. The current study investigated whether mildly elevated circulating unconjugated bilirubin (UCB) is negatively associated with multiple thrombotic risk factors including platelet activity, hemostatic function, and inflammation in individuals with GS. Blood samples were collected from matched GS and control subjects (14 per group). Activation-dependent platelet surface marker expression of PAC-1 (binds to GPIIb/IIIa surface receptors on activated platelets) and CD62P (marker for P-selectin released from activated degranulated platelets) was assessed in adenosine diphosphate (ADP)-stimulated platelets using flow cytometry. Exogenous agonists, ADP, collagen, and arachidonic acid (AA), were used to stimulate platelet aggregation. A statistically significant decrease in the expression of P-selectin (P = 0.030) on activated platelets was observed in GS subjects. Collagen and AA-induced platelet aggregation were significantly (P = 0.018; P = 0.032 for respective agonists) reduced in GS versus control group. Elevated UCB (P = 0.001) and high density lipoprotein (P = 0.033) in addition to reduced low density lipoprotein (P = 0.024) and high sensitive C-reactive protein (P = 0.043) were also observed in GS when compared to the control group. Reduced P-selectin expression suggests decreased platelet activation-dependent degranulation, while reduced platelet aggregation by AA and collagen indicates a quantitative decrease in platelet aggregation consequently targeting the cyclooxygenase-1 and GP VI pathways, respectively. These findings are the first to demonstrate that the activation of platelets is mildly inhibited in individuals with GS, an effect that might contribute to protection from platelet hyperactivation-induced thrombosis and thus cardiovascular mortality in individuals with benign hyperbilirubinemia.en_US
dc.description.peerreviewedYesen_US
dc.languageEnglishen_US
dc.publisherTaylor & Francisen_US
dc.relation.ispartofpagefrom1en_US
dc.relation.ispartofpageto7en_US
dc.relation.ispartofjournalPlateletsen_US
dc.subject.fieldofresearchClinical Sciences not elsewhere classifieden_US
dc.subject.fieldofresearchcode110399en_US
dc.titleMildly elevated unconjugated bilirubin is associated with reduced platelet activation-related thrombogenesis and inflammation in Gilbert's syndromeen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.facultyGriffith Health, School of Medicineen_US
gro.description.notepublicThis publication has been entered into Griffith Research Online as an Advanced Online Version.en_US
gro.hasfulltextNo Full Text


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