Increased Placental Apoptosis in Maternal Food Restricted Gestations: Role of the Fas Pathway |
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| Authors: | L. Belkacemi C.H. Chen M.G. Ross M. Desai |
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| Affiliation: | 1. LABioMed Research Institute at Harbor-UCLA Medical Center, Los Angeles, CA 90502, USA;2. Perinatal Research Laboratories, David-Geffen School of Medicine at UCLA, Los Angeles, CA 90502, USA;3. Department of Obstetrics and Gynecology, Chang Gung Memorial Hospital-Chia Yi Medical Center, Taiwan;1. Programa de Anatomía y Biología del Desarrollo, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile;2. Programa de Biología Celular y Molecular, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile;3. Programa de Farmacología Molecular y Clínica, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile;4. Departamento de Estomatología, Facultad de Ciencias de la Salud, Universidad de Talca, Chile;1. Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, United States;2. Emory University, Atlanta, GA, United States;3. Division of Maternal Fetal Medicine/ Obstetrics and Gynecology, University of Chicago Medical Center, Chicago, IL, United States;1. Bulent Ecevit University, Faculty of Medicine, Department of Biochemistry, Zonguldak, Turkey;2. Bulent Ecevit University, Faculty of Medicine, Department of Pathology, Zonguldak, Turkey;3. Bulent Ecevit University, Faculty of Medicine, Department of Gynaecology and Obstetrics, Zonguldak, Turkey;1. Obstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and Gynaecology, University of Melbourne, Mercy Hospital for Women, Heidelberg, Victoria, Australia;2. Mercy Perinatal Research Centre, Mercy Hospital for Women, Heidelberg, Victoria, Australia;1. Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS, USA;2. Saint Luke''s Health System, Department of Maternal and Fetal Medicine, Kansas City, MO, USA;3. The Center for Women''s Health, Overland Park, KS, USA |
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| Abstract: | ![]()
The placenta has a pivotal role, shuttling nutrients to the developing fetus and producing hormones essential to pregnancy. Maternal food restriction (MFR) during pregnancy results in growth restricted newborns, a consequence attributed primarily to maternal nutrient supply. We hypothesized that MFR further compromises fetal growth by decreased placental growth or increased placental apoptosis. We determined the potential pathway (Fas–Fas-ligand; Fas-FasL) of placental apoptosis in MFR pregnancies. We assessed the two morphologically and functionally distinct zones (basal and labyrinth) at embryonic age 20 (E20) in ad libitum fed controls (AdLib) and 50% MFR placentas. We studied fetuses and placentas from both proximal and mid-horn positions to evaluate any differential impact by MFR. Placenta apoptosis was quantified using terminal dUTP nick-end labeling (TUNEL) assay and the data were compared to immunodetection of cleaved caspase-3, Fas and FasL followed by Western blot quantification of Fas, FasL, caspase-8 and -3, tBID, and poly-ADP-ribose polymerase (PARP). MFR reduced maternal, fetal and placental basal and labyrinth weights. The results suggest that the increased apoptosis may be mediated, in part, via Fas pathway and the defective placental development in the MFR may be a major contributor to the decreased fetal growth. |
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