The following is a summary of “Placental transcriptomic signatures of spontaneous preterm birth,” published in the January 2023 issue of Obstetrics and Gynecology by Paquette, et al.
Most preterm births are caused by spontaneous preterm birth, which has serious consequences for infants and children. When compared to preterm births that are medically indicated, this subtype of preterm birth accounted for an increasing share of all preterm births; nonetheless, omics investigations had seldom examined it. The placenta plays a significant role in regulating the health of the fetus and the infant. The placental transcriptome can shed light on the pathologic alterations resulting in spontaneous premature delivery. For a study, researchers sought to find genes whose placental expression was linked to spontaneous preterm birth (including early preterm and late preterm birth).
From placental samples obtained from the Conditions Affecting Neurocognitive Development and Learning in Early Childhood and the Global Alliance to Prevent Prematurity & Stillbirth investigations, the ECHO PATHWAYS consortium extracted RNA. By using RNA sequencing, placental transcriptome data were collected. To calculate the variations in placental gene expression between term birth and spontaneous preterm delivery, linear models were fitted (including gestational age subgroups defined by the American College of Obstetricians and Gynecologists). Numerous confounding factors, such as labor status, cohort, and RNA sequencing batch, were considered while creating the models. Patients with induced labor, chorioamnionitis, multiple fetal gestations, or medical reasons for premature birth were not included in the research. In 48 preterm and 540 term samples from the combined cohort, 14,023 genes’ gene expression levels were recorded. At a false discovery rate-adjusted P value of<.05., genes and pathways were deemed statistically significantly distinct from one another.
They discovered 1,728 genes in total whose placental expression was linked to spontaneous preterm delivery; early preterm samples showed larger variations in expression than late preterm samples when compared to full-term data. Nine of them, including IL1B, ALPL, and CRLF1, showed a substantial drop in expression in both early and late spontaneous preterm delivery. The genes were most strongly associated with early spontaneous preterm birth. They noted lower expression of genes related to immunological signaling, signal transduction, and endocrine function in early and late preterm samples.
With a strong confounding correction, the study thoroughly evaluated the variations in the placental transcriptome linked to spontaneous preterm delivery. Since they found several genes and pathways for which the placental and chorioamniotic membrane expression was previously connected with prematurity, including IL1B, the results of our investigation were in agreement with the known etiology of spontaneous preterm delivery. The etiology of spontaneous preterm delivery may be connected to the reduced expression of critical signaling pathways that are crucial for placental development and function, which they found. They discovered elevated gene expression in metabolic pathways that are only linked with early preterm birth. These metabolic and signaling pathways may offer indicators and therapeutically targetable pathways. The study’s findings might be utilized to comprehend the pathologic alterations that underlie preterm placentas, which would help guide and advance clinical obstetrics practice.