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Maternal Smoking,Intrauterine Growth Restriction,and Placental Apoptosis
Authors:Christina Vogt?Isaksen  author-information"  >  author-information__contact u-icon-before"  >  mailto:christina.isaksen@medisin.ntnu.no"   title="  christina.isaksen@medisin.ntnu.no"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author,Rigmor?Austgulen,Lisa?Chedwick,Pal?Romundstad,Lars?Vatten,Catherine?Craven?
Affiliation:(1) Department of Pathology and Medical Genetics/National Center for Fetal Medicine, St. Olav"rsquo"s Hospital, 7006, Trondheim, Norway;(2) Department of Laboratory Medicine, Children"rsquo"s and Women"rsquo"s 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:Pregnantwomen who smoke are at greater risk of delivering a growth-restricted infantthan nonsmoking mothers. We wanted to see if apoptosis could be involved in themechanisms behind smoke-induced growth restriction, and our aim was to compareapoptosis in the placenta of smoking mothers giving birth to growth-restrictedinfants and nonsmoking mothers with infants of appropriate weight. The projectwas conducted at the Magee—Womens Hospital and Magee—WomensResearch Institute, University of Pittsburgh, PA. Histological sections from 20placentas were selected from smoking mothers who had given birth tosmall-for-gestational-age infants (birth weight le 2 SD). The controlswere gestational-age matched nonsmoking mothers with infants havingappropriate-for-gestational-age weight. The TUNEL method was used todemonstrate DNA fragmentation in nuclei, and a monoclonal antibody M30,specific for a neo-epitope on cytokeratin 18, was used to identify apoptoticepithelial cells. The positive nuclei (TUNEL) and positive cells (M30-positivecytoplasm) were counted blindly both in villous tissue and in decidual/basalplate tissue. M30-positive cells in villous tissues were significantlyincreased in placentas from smoking mothers compared to nonsmoking mothers.When evaluated by the TUNEL method, the difference between the two groups ofwomen was not significant. Our study shows that apoptosis was increased in theplacentas of smoking mothers with growth-restricted infants. The differencebetween the two groups was mainly in the syncytiotrophoblast layer and inconnection with perivillous fibrin deposition. Cigarette smoke with reductionin blood flow has previously been shown to increase apoptosis, and it ispossible that this could be one of the mechanisms playing a role in the growthrestriction.The work was performed at Magee—Womens Hospital andMagee—Womens Institute, University of Pittsburgh, Pittsburgh, PA, USA.1; daggerDeceased April 1, 2003, former address: Valley View Medical Center, 595 South75 East, Cedar City, UT 84720, USA.
Keywords:apoptosis  growth restriction  placenta  pregnancy  smoking
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