Skip to main content
SMFM 2025 Pregnancy Meeting Main banner
Final Program


Program Book
Icon Legend
Presentation Icons
Additional registration fee required
Additional registration fee required
CME Credit Offered
CME Credit Offered
Abstract Award
Abstract Award
Poster Icons
Additional registration fee required
Additional registration fee required
Faculty have requested this content not be shared on social media
Faculty have requested this content not be shared on social media
CME Credit Offered
CME Credit Offered
Abstract Award
Abstract Award
Back

Oral Concurrent Session 1 - Equity, Public Health, and Policy

Oral Concurrent Sessions

Oral Concurrent Session 1 - Equity, Public Health, and Policy

(9) Dysregulated gene expression in placentas with exposure to persistent maternal socioeconomic disadvantage

Thursday, January 30, 2025
1:30 PM – 1:45 PM  
Location: Aurora Ballroom A, Lobby Level
Objective: Persistent socioeconomic disadvantage is associated with many adverse health outcomes across the lifespan. One hypothesis is these risks start during gestation from hardship-related changes in placental gene expression. Studies in animal models have yielded results consistent with this hypothesis, but it has yet to be tested in large, diverse human cohorts.

Study Design: 605 patients with singleton pregnancies were recruited during their first trimester. Socioeconomic status (SES) data was collected using a standardized interview, and disadvantage was quantified by educational attainment and occupational prestige. Biopsies from distinct cotyledons of the placenta’s chorionic villous layer were collected < 2 hours from delivery and used for genome-wide expression profiling via RNA-Seq on an Illumina NovaSeq X Plus. Data were analyzed with linear mixed models, adjusted for maternal age, race, ethnicity, BMI, obstetric risk, delivery mode, and fetal sex.

Results: 449 participants delivered at term and had complete data. At a threshold of 1.50 fold-change, analyses identified 1,859 transcripts that were differentially expressed across the 4 standard deviation range of SES. 1,311 transcripts were upregulated in conjunction with SES disadvantage and 548 were downregulated. Bioinformatic analyses yielded indications that SES disadvantage was associated with upregulated pro-inflammatory transcriptional pathways (those anchored by GATA, STAT, MAF, and IRF) in fetal myeloid cells, but also with downregulation of trophoblast transcriptional pathways involved in fetal organ maturation (those anchored by PBX, c-ETS, ELK1, PAX, and CREB).

Conclusion: These results suggest molecular correlates of maternal disadvantage during pregnancy are present in mRNA from the placenta chorionic villous layer demonstrating SES disparities in placental biology. Multiple dimensions of placental gene expression were dysregulated with exposure to SES disadvantage. Future work should focus on interventions that reduce SES disadvantage before and during pregnancy, and evaluate their impact on pregnancy outcomes and placental biology.