PMID- 29409879 OWN - NLM STAT- MEDLINE DCOM- 20180314 LR - 20180513 IS - 1090-2104 (Electronic) IS - 0006-291X (Linking) VI - 496 IP - 4 DP - 2018 Feb 19 TI - Soluble FLT-1 rules placental destiny. PG - 1243-1249 LID - S0006-291X(18)30209-2 [pii] LID - 10.1016/j.bbrc.2018.01.180 [doi] AB - INTRODUCTION: Placenta previa is an abnormality in which the placenta covers the internal uterine os, and it can cause serious morbidity and mortality in both mother and fetus due to catastrophic hemorrhage. Some pregnant women recover from placenta previa due to a phenomenon called "migration." However, the mechanism of "migration" of the placenta has not been elucidated. METHODS: Human placentas were collected from patients with placenta previa and those with no abnormal placentation (control). A microarray analysis was performed to detect the genes up- or down-regulated only in the caudal part in the previa group. Specific mRNA expression was evaluated using real-time quantitative reverse transcription PCR (qRT-PCR). Unilateral uterine artery ablation of 8.5 dpc mice was performed to reproduce the reduction of placental blood supply, and weights of the placentas and fetuses were evaluated in 18.5 dpc. Specific mRNA expression was also evaluated in mice placentas. RESULTS: According to the result of the microarray analysis, we focused on soluble fms-like tyrosine kinase-1 (sFLT-1) and hypoxia-inducible factor-1 (HIF-1) alpha. The sFLT-1 expression level is locally high in the caudal part of the human placenta in patients with placenta previa. In mice experiments, the weights of the placentas and fetuses were significantly smaller in the ablation side than those in the control side, and the sFlt-1 expression level was significantly higher in the ablation side than in the control side. DISCUSSION: Our study suggests that "migration" of the placenta is derived from placental degeneration at the caudal part of the placenta, and sFlt-1 plays a role in this placental degeneration. CI - Copyright (c) 2018 Elsevier Inc. All rights reserved. FAU - Yamashita, Michiko AU - Yamashita M AD - Department of Obstetrics and Gynecology, Graduate School of Medicine, Osaka University, Osaka, Japan. Electronic address: uri_ton@hotmail.com. FAU - Kumasawa, Keiichi AU - Kumasawa K AD - Department of Obstetrics and Gynecology, Graduate School of Medicine, Osaka University, Osaka, Japan. Electronic address: kumasawa@gyne.med.osaka-u.ac.jp. FAU - Nakamura, Hitomi AU - Nakamura H AD - Department of Obstetrics and Gynecology, Graduate School of Medicine, Osaka University, Osaka, Japan. Electronic address: hitomi@gyne.med.osaka-u.ac.jp. FAU - Kimura, Tadashi AU - Kimura T AD - Department of Obstetrics and Gynecology, Graduate School of Medicine, Osaka University, Osaka, Japan. Electronic address: tadashi@gyne.med.osaka-u.ac.jp. LA - eng PT - Journal Article DEP - 20180131 PL - United States TA - Biochem Biophys Res Commun JT - Biochemical and biophysical research communications JID - 0372516 RN - 0 (Hypoxia-Inducible Factor 1, alpha Subunit) RN - EC 2.7.10.1 (FLT1 protein, human) RN - EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1) SB - IM EIN - Biochem Biophys Res Commun. 2018 May 9;:. PMID: 29753561 MH - Adult MH - Animals MH - Female MH - Humans MH - Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism MH - In Vitro Techniques MH - Mice, Inbred ICR MH - Middle Aged MH - Organ Specificity MH - Placenta/*metabolism MH - Placenta Previa/*mortality MH - *Placentation MH - Pregnancy MH - Species Specificity MH - Tissue Distribution MH - Vascular Endothelial Growth Factor Receptor-1/*metabolism OTO - NOTNLM OT - Placenta previa OT - Placental migration OT - Soluble fms-like tyrosine kinase-1 (sFLT-1) EDAT- 2018/02/08 06:00 MHDA- 2018/03/15 06:00 CRDT- 2018/02/08 06:00 PHST- 2018/01/20 00:00 [received] PHST- 2018/01/30 00:00 [accepted] PHST- 2018/02/08 06:00 [pubmed] PHST- 2018/03/15 06:00 [medline] PHST- 2018/02/08 06:00 [entrez] AID - S0006-291X(18)30209-2 [pii] AID - 10.1016/j.bbrc.2018.01.180 [doi] PST - ppublish SO - Biochem Biophys Res Commun. 2018 Feb 19;496(4):1243-1249. doi: 10.1016/j.bbrc.2018.01.180. Epub 2018 Jan 31.