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Prematurity

Poster Session 2

(422) Differences in placental gene expression in term and preterm birth

Tuesday, February 13, 2024
3:30 PM – 5:00 PM  
Location: Prince George's Exhibit Hall CDE, Lower Atrium Level
Objective: We used novel placental gene expression analysis to compare placental gene expression of preterm birth (PTB) vs term birth (TB) participants and evaluate underlying biological mechanisms of PTB.

Study Design: This is a secondary analysis of a prospective randomized controlled trial of a racially diverse, low-income sample. Genome-wide mRNA profiles from fresh placental villous tissues were analyzed to identify transcripts showing >2-fold differential expression in spontaneous PTB (sPTB) vs TB, controlling for potential confounders, including maternal age, first prenatal BMI, race, ethnicity, and smoking. Parallel analyses examined indicated PTB (iPTB) vs TB with a >1.5-fold differential to accommodate the more modest transcriptomic correlates.

Results: Of the 700 placentas biopsied, 69 were PTB: 28 sPTB and 41 iPTB. 493 differently expressed genes between sPTB vs TB indicated increased activity of multiple gene regulation pathways (Figure 1), including hypoxia-induced pathways (HIF2A↑66%, p< .001), innate immune response pathways (NF-kB↑56%, p=.033; IRF3↑80%, p< .001; MAF↑23%, p=.004), and neural signaling (CREB↑195%, p< .001). Other inflammatory pathways were conversely down-regulated (AP1↓36%, p< .001; STAT↓45%, p< .001).  Transcript origin analyses implicated myeloid dendritic cells and non-classical monocytes in mediating differential gene expression in sPTB placentas (both p< .05). Most of these patterns were not seen in iPTB placentas (no significant difference in HIF2A, NF-kB, IRF3, AP1, CREB), although iPTB showed elevated MAF activity (↑25%, p< .001) and indicated dendritic cell and monocyte activity (both p< .010). 

Conclusion: Placental tissue from sPTB showed activation of multiple gene regulation pathways involved in hypoxia, innate immune function, and neural signaling, and indicated myeloid lineage immune cell activation. Activation of these transcription control pathways are distinct to sPTB compared to iPTB and independent of maternal characteristics. These gene regulatory alterations may illuminate novel biological pathways underlying sPTB.