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Maternal Smoking,Intrauterine Growth Restriction,and Placental Apoptosis
Authors:Email author" target="_blank">Christina Vogt?IsaksenEmail author  Rigmor?Austgulen  Lisa?Chedwick  Pal?Romundstad  Lars?Vatten  Catherine?Craven?
Institution:(1) Department of Pathology and Medical Genetics/National Center for Fetal Medicine, St. Olavrsquos Hospital, 7006, Trondheim, Norway;(2) Department of Laboratory Medicine, Childrenrsquos and Womenrsquos Health, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway;(3) Institute of Cancer Research and Molecular Biology, Norwegian University of Science and Technology, Trondheim, Norway;(4) Magee—Womens Research Institute, University of Pittsburgh, Pittsburgh, PA, USA;(5) Institute of Community Medicine and General Practice, Norwegian University of Science and Technology, Trondheim, Norway
Abstract:Pregnant women who smoke are at greater risk of delivering a growth-restricted infant than nonsmoking mothers. We wanted to see if apoptosis could be involved in the mechanisms behind smoke-induced growth restriction, and our aim was to compare apoptosis in the placenta of smoking mothers giving birth to growth-restricted infants and nonsmoking mothers with infants of appropriate weight. The project was conducted at the Magee—Womens Hospital and Magee—Womens Research Institute, University of Pittsburgh, PA. Histological sections from 20 placentas were selected from smoking mothers who had given birth to small-for-gestational-age infants (birth weight le 2 SD). The controls were gestational-age matched nonsmoking mothers with infants having appropriate-for-gestational-age weight. The TUNEL method was used to demonstrate DNA fragmentation in nuclei, and a monoclonal antibody M30, specific for a neo-epitope on cytokeratin 18, was used to identify apoptotic epithelial cells. The positive nuclei (TUNEL) and positive cells (M30-positive cytoplasm) were counted blindly both in villous tissue and in decidual/basal plate tissue. M30-positive cells in villous tissues were significantly increased in placentas from smoking mothers compared to nonsmoking mothers. When evaluated by the TUNEL method, the difference between the two groups of women was not significant. Our study shows that apoptosis was increased in the placentas of smoking mothers with growth-restricted infants. The difference between the two groups was mainly in the syncytiotrophoblast layer and in connection with perivillous fibrin deposition. Cigarette smoke with reduction in blood flow has previously been shown to increase apoptosis, and it is possible that this could be one of the mechanisms playing a role in the growth restriction.The work was performed at Magee—Womens Hospital and Magee—Womens Institute, University of Pittsburgh, Pittsburgh, PA, USA. 1; dagger Deceased April 1, 2003, former address: Valley View Medical Center, 595 South 75 East, Cedar City, UT 84720, USA.
Keywords:apoptosis  growth restriction  placenta  pregnancy  smoking
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