PMID- 37718409 OWN - NLM STAT- MEDLINE DCOM- 20230919 LR - 20231122 IS - 1528-3658 (Electronic) IS - 1076-1551 (Print) IS - 1076-1551 (Linking) VI - 29 IP - 1 DP - 2023 Sep 18 TI - Regulation of sexually dimorphic placental adaptation in LPS exposure-induced intrauterine growth restriction. PG - 114 LID - 10.1186/s10020-023-00688-5 [doi] LID - 114 AB - BACKGROUND: Sexual dimorphism in placental physiology affects the functionality of placental adaptation during adverse pregnancy. Defects of placental function compromise fetal programming, affecting the offspring's adult life. However, studies focusing on the relationship between sex-specific placental adaptation and consequent fetal maldevelopment under sub-optimal uterus milieu are still elusive. METHODS: Here, we investigated the effects of maternal lipopolysaccharide (LPS) exposure between placental sex. Pregnant ICR mice received intraperitoneal injection of phosphate-buffered saline or 100, 200, and 400 microg/kg LPS on the gestational day (GD) 15.5. To determine whether prenatal maternal LPS exposure resulted in complicated pregnancy outcomes, survival rate of embryos was calculated and the growth of embryos and placentas was examined. To elucidate global transcriptomic changes occurring in the placenta, total RNA-sequencing (RNA-seq) was performed in female and male placentas. RESULTS: LPS administration induced placental inflammation in both sexes at GD 17.5. Prenatal infection resulted in growth retardation in both sexes of embryos, and especially more prevalently in male. Impaired placental development was observed in a sex-specific manner. LPS 400 microg/kg reduced the percentage area of the labyrinth in females and junctional zone in males, respectively. RNA-sequencing revealed widespread sexually dimorphic transcriptional changes in placenta. In particular, representative changes were involved in biological processes such as trophoblast differentiation, nutrient/ion transporter, pregnancy, and immune system. CONCLUSIONS: Our results present the sexually dimorphic responses of placental physiology in intrauterine growth restriction model and provide tentative relationship further to be elucidated between sex-biased placental functional change and long-term effects on the offspring's later life. CI - (c) 2023. The Feinstein Institute for Medical Research. FAU - Jeong, Da Som AU - Jeong DS AD - Department of Anatomy, Embryology Laboratory, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea. AD - Department of Internal Medicine, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea. FAU - Lee, Ji-Yeon AU - Lee JY AD - Vivozon, Inc, Kolon Digital Tower3, 49, Achasan-ro, Seongdong-gu, Seoul, Republic of Korea. FAU - Kim, Myoung Hee AU - Kim MH AD - Department of Anatomy, Embryology Laboratory, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea. mhkim1@yuhs.ac. FAU - Oh, Ji Hoon AU - Oh JH AUID- ORCID: 0000-0001-5652-1452 AD - Department of Biological Sciences, Keimyung University College of Natural Sciences, Daegu, 42601, Republic of Korea. dr.jihoonoh@gmail.com. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20230918 PL - England TA - Mol Med JT - Molecular medicine (Cambridge, Mass.) JID - 9501023 RN - 0 (Lipopolysaccharides) RN - 63231-63-0 (RNA) SB - IM MH - Female MH - Male MH - Pregnancy MH - Mice MH - Animals MH - Humans MH - Mice, Inbred ICR MH - *Fetal Growth Retardation/chemically induced MH - *Lipopolysaccharides MH - Placenta MH - RNA PMC - PMC10506314 OTO - NOTNLM OT - Intrauterine growth restriction OT - Placenta transcriptome OT - Placental adaptation OT - Prenatal maternal stress OT - Sexual dimorphism COIS- Author Ji-Yeon Lee is employed by Vivizon Co. The remaining authors declare that the research was conducted without any commercial or financial relationships that could be construed as a potential conflict of interest. EDAT- 2023/09/18 00:41 MHDA- 2023/09/19 06:42 PMCR- 2023/09/18 CRDT- 2023/09/17 23:13 PHST- 2022/11/20 00:00 [received] PHST- 2023/06/15 00:00 [accepted] PHST- 2023/09/19 06:42 [medline] PHST- 2023/09/18 00:41 [pubmed] PHST- 2023/09/17 23:13 [entrez] PHST- 2023/09/18 00:00 [pmc-release] AID - 10.1186/s10020-023-00688-5 [pii] AID - 688 [pii] AID - 10.1186/s10020-023-00688-5 [doi] PST - epublish SO - Mol Med. 2023 Sep 18;29(1):114. doi: 10.1186/s10020-023-00688-5.