title: Assisted reproduction causes placental maldevelopment and dysfunction linked to reduced fetal weight in mice.
abstract: Compelling evidence indicates that stress in utero, as manifested by low birth weight (LBW), increases the risk of metabolic syndrome in adulthood. Singletons conceived by assisted reproductive technology (ART) display a significant increase in LBW risk and ART offspring have a different metabolic profile starting at birth. Here, used mouse as a model, we found that ART resulted in reduced fetal weight and placental overgrowth at embryonic day 18.5 (E18.5). The ART placentae exhibited histomorphological alterations with defects in placental layer segregation and glycogen cells migration at E18.5. Further, ART treatments resulted in downregulation of a majority of placental nutrient transporters and reduction in placental efficiency. Moreover, the ART placentae were associated with increased methylation levels at imprinting control regions of H19, KvDMR1 and disrupted expression of a majority of imprinted genes important for placental development and function at E18.5. Our results from the mouse model show the first piece of evidence that ART treatment could affect fetal growth by disrupting placental development and function, suggests that perturbation of genomic imprinting resulted from embryo manipulation may contribute to these problems.
authors.affiliation: 1] Department of Obstetrics and Gynecology, Tangdu Hospital, the Fourth Military Medical University, Xi'an 710038, China [2] Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100080, People's Republic of China.
authors.forename: Shuqiang
authors.initials: S
authors.lastname: Chen
authors.affiliation: Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100080, People's Republic of China.
authors.forename: Fang-zhen
authors.initials: FZ
authors.lastname: Sun
authors.affiliation: Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100080, People's Republic of China.
authors.forename: Xiuying
authors.initials: X
authors.lastname: Huang
authors.affiliation: Department of Obstetrics and Gynecology, Tangdu Hospital, the Fourth Military Medical University, Xi'an 710038, China.
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Wang
authors.affiliation: Shaanxi Institute for Food and Drug Control, Xi'an 710038, People's Republic of China.
authors.forename: Na
authors.initials: N
authors.lastname: Tang
authors.affiliation: Department of Obstetrics and Gynecology, Tangdu Hospital, the Fourth Military Medical University, Xi'an 710038, China.
authors.forename: Baoyi
authors.initials: B
authors.lastname: Zhu
authors.affiliation: Department of Obstetrics and Gynecology, Tangdu Hospital, the Fourth Military Medical University, Xi'an 710038, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Li
mesh_terms: D000818:Animals; D005260:Female; D020567:Fetal Weight; D005333:Fetus / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D010920:Placenta; D010922:Placenta Diseases / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D010929:Placentation; D011247:Pregnancy; D027724:Reproductive Techniques, Assisted / Q000009:adverse effects*