title: Folate ameliorates dexamethasone-induced fetal and placental growth restriction potentially via improvement of trophoblast migration.
abstract: Overexposure to prenatal dexamethasone (Dex) leads to small placental and fetal size and the alteration of fetal programming. Folate plays important roles in processes associated with successful pregnancy, including angiogenesis and trophoblast invasion. Placental folate transport is altered with prenatal Dex administration. The purpose of this study was to investigate the protective role of maternal folate administration in placentas exposed to Dex. In vitro, four groups of C57BL/6J pregnant mice were utilized: 1) normal drinking water+Saline injection group (NN); 2) normal drinking water+Dex injection group (ND); 3) drinking water with folate+Saline injection group (FN); and 4) drinking water with folate+Dex injection group (FD). In vivo, four treatment groups of the human extravillous trophoblast HTR-8/SVneo cells were classified: 1) control (NN); 2) Dex treatment (ND); 3) folate treatment (FN); and 4) folate and Dex treatment (FD). The results showed the maternal folate increases the placental size, birth weight, and expression of matrix metalloproteinases 9 (MMP9) in a mice model of Dex overexposure. In human extravillous trophoblast HTR8/SVneo, folate ameliorated the Dex-induced supress of cell migration and improved the expression/activity of MMP2 and MMP9. In conclusion, folate might be a potential therapy intervention to reduce the adverse effects of prenatal Dex exposure partially via improved trophoblast migration.
authors.affiliation: Department of Obstetrics, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine Shanghai 200040, China.
authors.forename: Linfang
authors.initials: L
authors.lastname: Zhou
authors.affiliation: Department of Obstetrics, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine Shanghai 200040, China.
authors.forename: Ai
authors.initials: A
authors.lastname: Zhang
authors.affiliation: Department of Obstetrics, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine Shanghai 200040, China.
authors.forename: Kai
authors.initials: K
authors.lastname: Wang
authors.affiliation: Department of Obstetrics, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine Shanghai 200040, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Zhou
authors.affiliation: Department of Obstetrics, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine Shanghai 200040, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Duan
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000009:adverse effects*; D002460:Cell Line; D002465:Cell Movement / Q000187:drug effects; D003907:Dexamethasone / Q000009:adverse effects*; D004195:Disease Models, Animal; D005260:Female; D005317:Fetal Growth Retardation / Q000139:chemically induced / Q000517:prevention & control; D005492:Folic Acid / Q000494:pharmacology*; D006801:Humans; D051379:Mice; D008810:Mice, Inbred C57BL; D010920:Placenta / Q000187:drug effects; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000517:prevention & control*; D060888:Real-Time Polymerase Chain Reaction; D014327:Trophoblasts / Q000187:drug effects*
chemical_list: D000893:Anti-Inflammatory Agents; D003907:Dexamethasone; D005492:Folic Acid
keywords: Placenta; dexamethasone; fetal programming; folate