GENETIC PREDISPOSITION TO PRE-ECLAMPSIA: POLYMORPHISM OF GENES INVOLVED IN REGULATION OF ENDOTHELIAL FUNCTIONS
Mozgovaia EV, Malysheva OV, Ivashchenko TE, Baranov VS*
*Corresponding Author: Professor Dr. Vladislav S. Baranov, Laboratory of Prenatal Diagnosis of Inherited Disorders, D.O. Ott Research Institute of Obstetrics and Gynecology, Russian Academy of Medical Sciences, Mendeleevskaya line 3, St. Petersburg 199034, Russia; Tel/Fax: +07-812-328-0487; E-mail: baranov@vb2475. spb.edu
page: 19

INTRODUCTION

Pre-eclampsia (PE) is one of the most widespread complications of pregnancy. The frequency of the disease in Russia is about 20% of all pregnancies. Disturbances in blood circulation constitute the major pathogenic back­ground of typical PE symptoms, which include the classi­cal triad of edema, proteinuria and hypertension. Recent studies have shown that PE is a typical multifactorial dis­order with different pathogenic mechanisms underlying its final clinical manifestation

 

It is commonly accepted that PE results from the shal­low endovascular cytotrophoblastic invasion into the spiral placental arteries with subsequent reduced placental perfu­sion. The major source of these complications stems from preexisting maternal disorders sometimes not evident be­fore pregnancy such as hypertension, renal disease, obesity and diabetes. All of these predispose to PE through the common mechanism of endothelial dysfunction [1]. The combination of maternal and placental factors is particu­larly devastating. Oxidative stress has also been impli­cated in endothelial damage. One other major gene group of PE concerns intercellular interaction in placental devel­opment. Decidua is composed of cells, which can release bioactive compounds that interact with endothelial cells. This process is usually mediated through cytokines pro­duced by inflammatory cells and activated endothelial cells. Endothelial cell damage enhances the production of thrombin, platelet activating factor and other tissue hor­mones which affect endothelial cell permeability, expres­sion of adhesion molecules, down-regulation of endothe­lial nitric oxide synthetase activity, reduction of plasma fibrinolytic activity due to imbalance of tissue plasmin­ogen activator and its inhibitor.

Taking all these considerations into account, the fol­lowing polymorphic marker loci of genes responsible for predisposition to endothelial dysfunction were studied: tissue plasminogen activator (PLAT) and its inhibitor of type 1 (PAI-1), angiotensin-converting enzyme (ACE), endothelial nitric oxide synthetase (eNOS), cytokine tu­mor necrosis factor-a (TNF-a) and glutathione-S-trans­ferase P1 (GSTP1).




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