Abstract
Objective: The aim of this study was to investigate the endothelial protein C receptor (EPCR) gene A3 haplotype and plasma soluble EPCR (sEPCR) levels in Turkish pediatric arterial stroke patients. Materials and Methods: We analyzed 44 pediatric arterial stroke patients and 75 healthy controls. Following DNA isolation, genotyping of the A3 haplotype was determined via PCR and RFLP. Additionally, fasting sEPCR levels were determined via ELISA. Results: There wasn’t a significant difference in the sEPCR level between the control and patient groups, although the sEPCR level was higher in the patient group. We didn’t observe a difference in the distribution of the CC and CG/GG genotypes between the control and patient groups.Conclusion: Further study on sEPCR levels at the onset of pediatric stroke is needed in order to reach a more definitive conclusion.Conflict of interest:None declared.
Highlights
Stroke is a rare event in childhood, it constitutes approximately 33% of all pediatric thrombosis cases [1]
There wasn’t a significant difference in the soluble EPCR (sEPCR) level between the control and patient groups, the sEPCR level was higher in the patient group
Further study on sEPCR levels at the onset of pediatric stroke is needed in order to reach a more definitive conclusion
Summary
Stroke is a rare event in childhood, it constitutes approximately 33% of all pediatric thrombosis cases [1]. Active protein C (APC) is a major natural anticoagulant that limits the progression of the coagulation cascade via photolytic degradation of factor Va (FVa) and factor VIIIa (FVIIIa). Endothelial protein C receptor (EPCR) contributes to the interaction between thrombin-thrombomodulin and PC, and in this way this complex increases activation of PC [3]. EPCR is a 46-kDa endothelial cell-specific type-I transmembrane protein, it has a soluble form circulating in plasma [5,6]. The extracellular domain of EPCR is cleaved with a metalloprotease and the cleavage results in the formation of soluble EPCR (sEPCR) [7]. SEPCR binds to PC and APC with the same affinity as transmembrane EPCR [8]. SEPCR inhibits the anti-inflammatory, profibrinolytic, and anticoagulant effects of APC
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