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[Expression and significance of EPCR in plasma and placenta of patients with early onset severe preeclampsia].

Zhonghua Fu Chan Ke za Zhi 2016 September 26
Objective: To investigate the expression of endothelial protein C receptor(EPCR)and its roles in plasma and placenta of patients with early onset severe preeclampsia. Methods: Sixty cases of severe preeclampsia women who delivered in Xuzhou Maternity and Child Health Care Hospital from March 2014 to February 2016, were recruited, which included 30 cases with early onset severe preeclampsia(early onset group, gestational week <34 weeks)and 30 patients with late onset severe preeclampsia(late onset group, gestational week ≥34 weeks). Thirty cases of healthy late pregnant women at the same period(gestational week ≥34 weeks)were selected as control group. Immunohistochemistry SP method was applied to detect the expression of in EPCR placenta. Reverse transcription(RT)- PCR was used to detect the expression of EPCR mRNA in placenta. ELISA method was used to detect the levels of soluble EPCR(sEPCR)level in plasma of the pregnant women of the three groups. Results: The expression of EPCR in placenta mainly distributed in the membrane and cytoplasm of placental syncytiotrophoblasts and vascular endothelial cells, a few in the cell nucleus. The expression of EPCR in early onset group(57%, 17/30)was significantly lower than that in late onset group(93%, 28/30; χ(2)=25.165, P=0.001). The expression of EPCR in late onset group had no significant difference from that in control group(97%, 29/30; χ(2)=0.540, P= 0.910). The expression of EPCR mRNA in placenta of early onset group(0.40±0.07)was significantly lower than that in late onset group(0.91±0.06; t=-30.044, P=0.001), while there was no statistical difference of the expression of EPCR mRNA between the late onset group and the control group(0.92±0.07; t=-0.631, P=0.538). Plasma sEPCR level in early onset group, late onset group and control group were(231 ± 11),(124±6)and(121±4)μg/L respectively, which is higher in early onset group than that in late onset group(t=48.080, P=0.001). There was no statistical difference of plasma sEPCR level between the late onset group and the control group(t=2.534, P=0.100). Conclusions: The pathogenesis of early onset and late onset severe preeclampsia may be different. Decreased expression of EPCR in placenta may be associated with the pathogenesis of early onset severe preeclampsia.

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