This study investigates the toxic effect of harmful materials, unfiltered by the placenta,
on neonatal umbilical cord (UC) vessels, focusing on stress-induced adaptations in
transcriptional and translational processes. It aims to analyze changes in pathways
related to mRNA condensate formation, transcriptional regulation, and DNA damage response
under maternal smoking-induced stress. UC vessels from neonates born to smoking (Sm)
and nonsmoking mothers (Ctr) were examined. Immunofluorescence staining and confocal
microscopy assessed the localization of key markers, including Transcription Complex
Subunit 1 (CNOT1) and the largest subunit of RNA polymerase II enzyme (RPB1). Additionally,
markers of DNA damage response, such as Poly(ADP-ribose) polymerase-1, were evaluated.
In Sm samples, dissolution of CNOT1 granules in UC vessels was observed, potentially
aiding stalled translation and enhancing transcription via RPB1 assembly and translocation.
Control vessels showed predominant cytoplasmic RPB1 localization. Despite adaptive
responses, Sm endothelial cells exhibited significant damage, indicated by markers
like Poly(ADP-ribose) polymerase-1. Ex vivo metal treatment on control vessels mirrored
Sm sample alterations, emphasizing marker roles in cell survival under toxic exposure.
Maternal smoking induces specific molecular adaptations in UC vessels, affecting mRNA
condensate formation, transcriptional regulation, and DNA damage response pathways.
Understanding these intricate molecular mechanisms could inform interventions to improve
neonatal health outcomes and mitigate adverse effects of toxic exposure during pregnancy.
