Placental apoptosis and adhesion molecules expression in the placenta and the maternal placental bed of pregnancies complicated by fetal growth restriction with and without pre-eclampsia.
The aim of the study was to examine the expression of adhesion molecules VCAM-1 and ICAM-3 in placental tissue samples and placental bed (maternal decidual tissue) biopsies of pregnancies complicated by pre-eclampsia (PE) and fetal growth restriction (FGR), and to determine whether PE and FGR are associated with an increase in placental apoptosis. We studied placentas and placental bed samples of 49 third trimester pregnancies complicated by FGR (26 with associated PE, 23 without PE) and 25 normotensive healthy pregnant women. Placental apoptosis was assessed by the TUNEL method. Immunohistochemistry was used to assess expression of the VCAM-1 and ICAM-3. There was no significant difference in the staining intensity of VCAM-1 in placentas (p=0.472) and placental bed biopsies (p=0.754) of women delivering appropriate for gestational age and growth restricted fetuses (with and without associated PE). The amount of lymphocytes staining positively with ICAM-3 was significantly higher in both placental and placental bed biopsies of women delivering growth restricted fetuses compared with control pregnancies (p<0.001). Fetal growth restricted pregnancies with associated PE showed higher staining of ICAM-3 in placental compared with placental bed samples (p=0.049). In fetal growth restricted placentas, apoptotic nuclei were more abundant compared with control placentas (p<0.001). Increased expression of ICAM-3 on lymphocyte surface of both maternal and fetal side, suggests lymphocyte overactivation in PE and FGR. Increased placental apoptosis may play an important role in the pathogenesis or sequelae of PE.
Madazli
R
R
Department of Obstetrics, Gynecology and Pathology, Cerrahpasa Medical Faculty, University of Istanbul, Istanbul, Turkey. madazli@superonline.com
Benian
A
A
Ilvan
S
S
Calay
Z
Z
D000328:Adult; D015703:Antigens, CD / Q000032:analysis / Q000096:biosynthesis; D017209:Apoptosis / Q000502:physiology*; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000096:biosynthesis*; D003656:Decidua / Q000737:chemistry / Q000503:physiopathology*; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D006801:Humans; D010920:Placenta / Q000737:chemistry / Q000503:physiopathology*; D010922:Placenta Diseases / Q000209:etiology / Q000503:physiopathology; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy; D011263:Pregnancy Trimester, Third; D014591:Uterine Diseases / Q000209:etiology / Q000503:physiopathology; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis / Q000096:biosynthesis
D015703:Antigens, CD; D015815:Cell Adhesion Molecules; C483616:ICAM3 protein, human; D019010:Vascular Cell Adhesion Molecule-1