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Expression of Placental Regulatory Genes Is Associated with Fetal Growth

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Expression of Placental Regulatory Genes Is Associated with Fetal Growth City University of New York (CUNY) CUNY Academic Works Publications and Research Queens College 2017 Expression of Placental Regulatory Genes Is Associated with Fetal Growth Maya A. Deyssenroth Icahn School of Medicine at Mount Sinai Qian Li Icahn School of Medicine at Mount Sinai Marina Lacasaña Andalusian School of Public Health Yoko Nomura CUNY Queens College Carmen Marsit Emory University See next page for additional authors How does access to this work benefit ou?y Let us know! More information about this work at: https://academicworks.cuny.edu/qc_pubs/189 Discover additional works at: https://academicworks.cuny.edu This work is made publicly available by the City University of New York (CUNY). Contact: [email protected] Authors Maya A. Deyssenroth, Qian Li, Marina Lacasaña, Yoko Nomura, Carmen Marsit, and Jia Chen This article is available at CUNY Academic Works: https://academicworks.cuny.edu/qc_pubs/189 J. Perinat. Med. 2017; aop Maya A. Deyssenrotha, Qian Lia, Marina Lacasaña, Yoko Nomura, Carmen Marsit and Jia Chen* Expression of placental regulatory genes is associated with fetal growth DOI 10.1515/jpm-2017-0064 independent cohort (n = 306). Given that aberrant fetal Received February 25, 2017. Accepted May 31, 2017. growth may have long-lasting effects, our results suggest the potential utility of placental gene expression profiles as Abstract: The placenta is the principal organ regulating potential early markers of disease onset later in life. respiratory, nutritional, endocrine and metabolic functions on behalf of the developing fetus. Changes in gene expres- Keywords: Birth weight; gene expression, placenta. sion patterns of placenta-specific genes may influence fetal growth. We profiled the expression of 17 genes related to placenta functioning in term placentas (n = 677) to identify genes differentially expressed across birth weight catego- Introduction ries [small (SGA), appropriate (AGA) and large (LGA) for ges- Abnormal fetal growth, both undergrowth and overgrowth, tational age]. ABCG2, CEBPB, CRH, GCM1, GPC3, INSL4, PGF has been linked to adverse health outcomes later in life, and PLAC1 were inversely associated with LGA status, with including metabolic as well as cognitive and neurobehavio- odds ratios (ORs) and 95% confidence intervals (CI) ranging ral disorders [1–3]. The placenta is a transient organ situated from GCM1 (OR = 0.44, 95% CI: 0.29, 0.70) to CRH (OR = 0.73, at the maternal-fetal interface that regulates fetal growth 95% CI: 0.61, 0.88). NR3C1 was positively associated with and development by facilitating nutrient intake and waste LGA status (OR = 2.33, 95% CI: 1.43, 3.78). PLAC1 (OR = 0.66, removal, gas exchange, immune protection and neuroendo- 95% CI: 0.47, 0.92) and ABCG2 (OR = 0.63, 95% CI: 0.44, 0.91) crine functions on behalf of the developing fetus [4]. Given were additionally inversely associated with SGA status, and its important role in overseeing fetal development, placental PGF was positively associated with SGA status (OR = 1.59, gene expression patterns likely influence fetal growth. 95% CI = 1.08, 2.35). General trends were confirmed in an While several studies have reported associations between genes relevant to placental function and birth- aMaya A. Deyssenroth and Qian Li: These authors contributed weight, a proxy of fetal growth, many of these studies, equally to this work. including our own [5], focus on the relevance of imprinted *Corresponding author: Jia Chen, Icahn School of Medicine at Mount genes as placental regulators of fetal growth [5, 6]. Recent Sinai, One Gustave Levy Place, Box 1057, New York, NY 10029, USA; studies have also implicated the importance of a broad Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department range of non-imprinted genes, including genes involved of Pediatrics, Icahn School of Medicine at Mount Sinai, New in processes critical to the appropriate development of York, NY, USA; Department of Medicine, Hematology and Medical the placenta, such as differentiation, invasion, migra- Oncology, Icahn School of Medicine at Mount Sinai, New York, NY, tion and syncytialization, as well as genes that play a USA; and Department of Oncological Sciences, Icahn School of role in regulating maternal and fetal physiology, such as Medicine at Mount Sinai, New York, NY, USA, Tel.: +(212) 241-7592, E-mail: [email protected] neuroendocrine hormones and receptors [7]. However, Maya A. Deyssenroth and Qian Li: Department of Environmental studies to date linking regulators of placental function to Medicine and Public Health, Icahn School of Medicine at Mount Sinai, fetal growth have focused on a small subset of genes and New York, NY, USA. were limited by small sample sizes. Additional studies http://orcid.org/0000-0003-2913-2392 (M.A. Deyssenroth) have linked genes with known relevance to placental Marina Lacasaña: Andalusian School of Public Health, Granada, function to severe pregnancy complications, including Spain; CIBER of Epidemiology and Public Health (CIBERESP), Madrid, Spain; and Instituto de Investigación Biosanitaria (ibs. preeclampsia [8]. Given the important role of these genes GRANADA), Granada, Spain in regulating placental function, variability of these genes Yoko Nomura: Department of Environmental Medicine and Public in uncomplicated pregnancies may also bear relevance on Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA; fetal growth. Hence, a more comprehensive assessment Department of Psychology, Queens College, New York, NY, USA; and to explore genes relevant to a broader range of placental Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA functions in relation to fetal growth is warranted. Carmen Marsit: Department of Environmental Health, Emory We assembled a panel of 17 genes that were previ- University, Atlanta, GA, USA ously shown to play a critical role in placenta function. The 2 Deyssenroth et al., Expression of placental regulatory genes is associated with fetal growth Table 1: Panel of selected genes. Gene symbol Function Birth outcome ABCG2 Placental drug efflux transporter [9] Placental choriocarcinoma [10] CEBPB Transcription factor that induces decidualization of stromal cells [11] CRH Neuroendocrine hormone that likely plays an important role in gestational Predictor of pre-term birth; fetal growth length and parturition [12] restriction [13] CSH1 Vasodilator hormone [14] Altered expression in SGA and LGA infants [7, 13] CSHL1 Placental growth hormone; regulation of maternal/fetal metabolism [15] Altered expression in SGA and LGA infants [7] EPAS1 Placental angiogenic factor [16] Preeclampsia [17] GCM1 Trophoblast differentiation [18] Preeclampsia [19] GH2 Growth hormone; regulation of maternal/fetal metabolism [20] Altered expression and levels in SGA infants [7] GPC3 Trophoblast differentiation [21] Simpson-Golabi-Behmel fetal overgrowth syndrome [22] HIF1A Angiogenesis [23] Preeclampsia [24] INSL4 Trophoblast invasion and migration [25] Placenta accrete [26] NR3C1 Glucocorticoid receptor [27] Infant neurobehavior [28] Birth weight [29] NR3C2 Mineralocorticoid receptor; decidualization of stromal cells [30] PGF Placental angiogenic factor [31] Preeclampsia [32] PLAC1 Trophoblast invasion and migration into maternal decidua [33] Preeclampsia [34] PLAC4 Promotes syncytialization [35] Preeclampsia [35] PLAC8 Embryo development and implantation [36] selection was based on the following criteria: (1) highly/ As the RICHS population is predominantly Caucasian (78%) and uniquely expressed in placental tissue; (2) demonstrated oversampled for SGA and LGA infants, we conducted a replication study in the Stress in Pregnancy (SIP) study [38], an on-going urban functional role in fetal development (ABCG2, CEBPB, CRH, birth cohort that is more ethnically diverse and has a birth weight distri- CSHL1, GH2, INSL4, NR3C1, and PLAC8); or (3) demonstrated bution comparable to general population. The current study includes association with pregnancy complications (CSH1, EPAS1, mother-infant pairs recruited from prenatal clinics at the Icahn School GCM1, GPC3, HIF1A, NR3C2, PGF, PLAC1, and PLAC4). The of Medicine at Mount Sinai, New York Hospital of Queens and Queens selected genes and their relevance to placental function and College with available placental RNA. We restricted our analysis to sin- gleton pregnancies with gestational age ≥37 and maternal age ≥18 to birth outcomes are shown in Table 1. The objective of this match exclusion criteria implemented in the RICHS cohort (n = 307). study is to determine whether the expression levels of these “placenta regulatory genes” are associated with fetal growth. Placenta collection and RNA extraction Placental biopsies free of maternal decidua were excised from each of four quadrants midway between the cord insertion site and the Materials and methods placental rim within 2 h of delivery to optimize RNA integrity. The tis- sues were subsequently snap-frozen in liquid nitrogen, homogenized Study population with mortar and pestle, and stored at −80°C. RNA was extracted from RICHS placenta samples using the RNeasy mini kit (Qiagen, #74106) This study involves two independent birth cohorts. The first consisted and from SIP samples using the Maxwell simplyRNA Tissue Kit (Pro- of mother-infant pairs enrolled in the Rhode Island Child Health Study mega, #AS1280), following the manufacturer’s protocol. Extracted (RICHS) with available placental RNA (n = 684), as previously
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