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Fetus

Poster Session 4

(973) Placental gene expression: histologic evidence of maternal vascular malperfusion and small for gestational age newborns

Wednesday, February 14, 2024
1:00 PM – 2:30 PM  
Location: Prince George's Exhibit Hall CDE, Lower Atrium Level
Objective: Placental maternal vascular malperfusion (MVM) is a common pathologic histologic finding associated with adverse birth outcomes, including increased risk of delivering a small for gestational age (SGA, < 10% for GA) newborn. Measuring placental gene expression is an innovative approach to evaluate pathways that may increase SGA risk. We investigated differently expressed genes in MVM placentas from newborns with and without SGA.

Study Design: This is a secondary analysis of a prospective randomized controlled trial of a racially diverse, low-income sample. Placentas were collected at delivery. A trained perinatal pathologist conducted histologic placental evaluations. Our sample included placentas with ≥1 MVM lesion. Placental genome-wide mRNA profiles were analyzed to identify transcripts showing >1.5-fold differential expression in SGA vs non-SGA newborns, controlling for potential confounders, including GA at delivery, hypertension, newborn sex, race/ethnicity, smoking, and first prenatal BMI. TELiS analyzed transcription factor activity.

Results: Of 700 placentas assessed, 195 exhibited MVM. Among these, 32 (16.4%) delivered an SGA newborn. Bioinformatic analyses for participants with SGA newborns showed elevated activity of key pro-inflammatory signaling pathways (AP1↑15%, p=.013; NF-kB↑29%, p=.074) and unexpected reductions in hypoxia-signaling pathways (HIF1↓23%, p=.061; HIF2A↓10%, p=.009) (Figure 1). Exploratory results showed reduced activity of gene regulation pathways involved in tissue differentiation (GATA↑18%, p< .001; SMAD ↑9%, p< .001; FOXO↑35%, p< .001).

Conclusion: Participants with MVM lesions that delivered SGA newborns showed increased inflammatory pathway activity, decreased tissue differentiation and development pathway activity, and an unexpected decrease in hypoxia-associated pathways. These results suggest that inflammation and dysregulated tissue development may play a more prominent role than hypoxia in MVM associated with SGA newborns.