Stress-Induced Changes in Nucleocytoplasmic Localization of Crucial Factors in Gene Expression Regulation

被引:0
|
作者
Khamit, Ali [1 ]
Chakraborty, Payal [1 ,3 ]
Zahoran, Szabolcs [1 ,4 ]
Villanyi, Zoltan [1 ]
Orvos, Hajnalka [2 ]
Hermesz, Edit [1 ]
机构
[1] Univ Szeged, Fac Sci & Informat, Dept Biochem & Mol Biol, H-6701 Szeged, Hungary
[2] Univ Szeged, Albert Szent Gyorgy Med Sch, Dept Obstet & Gynecol, H-6701 Szeged, Hungary
[3] Calcutta Inst Pharmaceut Technol & Allied Hlth Sci, Dept Pharmacol, Howrah 711316, West Bengal, India
[4] Univ Geneva, Dept Cell Physiol & Metab, CH-1211 Geneva, Switzerland
关键词
blood vessels; CNOT1 (carbon catabolite repression-negative on TATA-less); fetal development; maternal smoking; PARP-1 (poly-(ADP-ribose) polymerase-1); rescue mechanism; RPB1 (the largest subunit of RNA polymerase II enzyme); RNA-POLYMERASE-II; POLY(ADP-RIBOSE) POLYMERASE; PROTEIN; PARP-1;
D O I
10.3390/ijms25073895
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
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页数:12
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