Immunohistochemical Localization and Quantitative Analysis of Placental VEGF and its Receptors KDR and Flt 1 in Patients with Pregnancy induced Hypertension

Abstract

Placental development requires extensive angiogenesis and the invasion of maternal decidua by trophoblasts. Failure of angiogenesis and trophoblast function lead to abnormal placental development which is associated with PILL a pregnancy-specific syndrome of hypertension and proteinuria. PIM is a multi-system disorder of pregnancy, which also involves several other symptoms, such as edema, disturbance of hemostasis. renal or liver failure and the HELLP syndrome. It can develop as an early onset (before 34 weeks) or late onset (after 34 weeks) of gestation. Adequate and organised interaction of vascular endothelial growth factor (VEGF) and its receptors are important for normal development and function of the placenta. Early pregnancy changes in VEGF and its receptors may thus identify women destined to develop P1H. There are no reliable tests to predict the development of P1H, remaining a major obstetric problem. Also, there is a paucity of information on VEGF and its receptors- VEGFR-I and VEGFR-2 placental expression and concentrations before and during the clinical onset of disease. Therefore, in this cross-sectional study, we investigated the expression of VEGF, membranous VEGFR-I and VEGFR-2 in 230 placental samples and evaluated the concentration of VEGF, soluble VEGFR-I and VEGFR-2 in 640 serum samples in PHI subgroups (Gestational hypertension, GHTN; Pre-eclampsia and Eclampsia) at early (5 34 weeks) and late (gt 34 weeks) onset of disease and control groups. newlineA significant up-regulation of VEGF (p=0.0001) and newlinemembranous VEGFR-1 (p).0001) expression and down-regulation of membranous VEGFR-2 (p=0.000I) was noticed in pre-eclampsia patients and in eclampsia patients as compared to their respective control groups. This denotes that VEGF and its receptors alter its expression as the severity of disease increases from GHTN to eclampsia, suggesting their altered regulation in the pathogenesis of NH. newline