To Study The Expression And Correlation Of Vascular Endothelial Growth Factor And Estrogen Receptor In Placenta Tissue

Preeclampsia is a disease which coexistence of pregnancy and high blood pressure. The incidence of the disease is related with the thickening of the blood and the increased vascular resistance. One of the major target organs of the disease is kidney. Clinical feature can be expressed as the maternal syndrome: hypertension and proteinuria, with or without other multi-system abnormalities. Recent studies have found that patients with hypertensive disorders in pregnancy women presence of shallow implantation of placenta, vascular recasting disorders, which resulting in placental ischemia and hypoxia. Hypoxia is an important factor in promoting the secretion of vascular endothelial growth factor(VEGF). The increased VEGF in body attempts to help promoting angiogenesis, increasing blood flow and oxygen-carrying, expanding blood vessels, lowing down blood pressure. However, the increased VEGF in the concentration of plasma may reflects an unsuccessful rescue mechanism. Further more, VEGF induces endothelial cells produce matrix metalloproteinases which promotes endothelin cleavage into a potent vasoconstrictor, increasing peripheral vascular resistance. This means that the increased production of VEGF in preeclampsia is not only an unsuccessful rescue mechanism, but also may actually lead to vasoconstriction state and the clinical syndrome. Secondly, because of the VEGF’s biological characteristics of endothelial repairing, preeclampsia increases VEGF’s production in the view of preeclampsia cause endothelial cells damage. but the increased circulating VEGF may increase the extravasation of plasma proteins and proteinuria. Soluble vascular endothelial growth factor receptor 1(soluble fims-like tyrosine kinase receptor 1, s Flt-1) is a receptor of VEGF: Flt-1’s splice variant, combined with VEGF in a soluble form but can not transcripte the signal, thus may close the excessive VEGF signal.So s Flt-1 reduces the damage to the placenta and fetus and play a protective role during preeclampsia. The VEGF’s expression in female’s reproductive system showes a change of cyclical, which suggests that prompted VEGF may be regulated by estrogen. However, the role of estrogen in the pathogenesis of preclampsia is not yet very clear, and the relationship between estrogen and VEGF needs further study.Objective:By studying the expressions of VEGF and ER in normal pregnancy, early-onset and late-onset severe preeclampsia placenta and the relevance between them, to explore their influences in onsetion and progression of preeclampsia.Methods:We randomly collect 90 cases of pregnant women deliveryed in the obstetrics of Second Hospital of Hebei Medical University between November 2013- March 2014. Among which 30 cases are in normal pregnancy group(A group), 30 cases are in late-onset severe preeclampsia group(group B), 30 cases are in early-onset severe preeclampsia group(group C). Immunohistoch-emistry method was used to detect the expression of VEGF and ER in normal pregnancy, early-onset and late-onset severe preeclampsia placenta. Using statistical software SPSS16.0 to statistically analysis the datas obtained by experiment, all datas are presented as mean ± standard deviation( x ± s). We use One-way analysis of variance compared among the groups, P <0.05 was considered statistically significant. Coefficient of product-moment correlation of pearson is applied to analyze the relationship between VEGF and ER’s expression, with a test level α <0.05.Result:1 Differences in age, body mass index, gestational age, termination age of pregnancy is not statistically significant between the three groups(P>0.05).2 VEGF’s average optical density in group A,group B, group C are 0.1453±0.023, 0.1566±0.025,0.1835±0.020. Compared with group A,VEGF’s expression in group B is increased, but there is no significant difference(P = 0.06).3 Compared with group A, VEGF’s expression is increased in group C,and the difference is significant between the two groups(P <0.001).4 VEGF’s expression in group C is increased compared with group B, and the difference between the two groups is significant(P <0.001).5 ER’s average optical density in group A,group B, group C are 0.1453±0.022, 0.1491±0.017, 0.1714±0.022.ER’s expression in group B is increased compared with group A, but there is no significant difference(P = 0.422).6 Compared with group A, ER’s expression is increased in group C, and the difference is significant between the groups(P <0.001).7 ER’s expression is increased in group C compared with group B, and the difference was significant between the two groups(P <0.001).8 ER’s expression and VEGF’s expression in the placenta were positively correlated(r = 0.231, P = 0.028 <0.05).Conclusion:1 VEGF and ER are both expressed in placenta tissue of normal pregnancy group, early-onset severe preeclampsia group and late-onset severe preeclampsia group. VEGF and ER’s expression gradually increased in normal pregnancy group, late-onset severe preeclampsia group and early onset severe preeclampsia group. The expression in early onset severe preeclampsia group was significantly more than the other two groups. Speculated that patients with preecalmpsia has something to do with VEGF and ER’s higher expression levels.2 The expression of VEGF and ER in early-onset preeclampsia group is increased compared to late-onset preeclampsia group, and the difference between the two groups is significant. Further study is needed to explor the different pathogens between the two groups.3 The expression of ER and VEGF’s expression in the placenta are positively correlated(r = 0.231, P = 0.028 <0.05). Speculate that ER may play an important role in promoting VEGF’s production.