Effects of In Utero EtOH Exposure on 18S Ribosomal RNA Processing: Contribution to Fetal Alcohol Spectrum Disorder.

18S Ribosomal RNA FASD Ribosomal RNA processing alcohol brain development exosomes neurons srRNA

Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
05 Sep 2023
Historique:
received: 08 08 2023
revised: 28 08 2023
accepted: 29 08 2023
medline: 28 9 2023
pubmed: 28 9 2023
entrez: 28 9 2023
Statut: epublish

Résumé

Fetal alcohol spectrum disorders (FASD) are leading causes of neurodevelopmental disability. The mechanisms by which alcohol (EtOH) disrupts fetal brain development are incompletely understood, as are the genetic factors that modify individual vulnerability. Because the phenotype abnormalities of FASD are so varied and widespread, we investigated whether fetal exposure to EtOH disrupts ribosome biogenesis and the processing of pre-ribosomal RNAs and ribosome assembly, by determining the effect of exposure to EtOH on the developmental expression of 18S rRNA and its cleaved forms, members of a novel class of short non-coding RNAs (srRNAs). In vitro neuronal cultures and fetal brains (11-22 weeks) were collected according to an IRB-approved protocol. Twenty EtOH-exposed brains from the first and second trimester were compared with ten unexposed controls matched for gestational age and fetal gender. Twenty fetal-brain-derived exosomes (FB-Es) were isolated from matching maternal blood. RNA was isolated using Qiagen RNA isolation kits. Fetal brain srRNA expression was quantified by ddPCR. srRNAs were expressed in the human brain and FB-Es during fetal development. EtOH exposure slightly decreased srRNA expression (1.1-fold;

Identifiants

pubmed: 37762017
pii: ijms241813714
doi: 10.3390/ijms241813714
pmc: PMC10531167
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NICHD NIH HHS
ID : R01 HD069238
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS092876
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS097846
Pays : United States
Organisme : Bill & Melinda Gates Foundation
ID : Gates Fund OPP1119489
Pays : United States

Déclaration de conflit d'intérêts

The authors declare no conflict of interests.

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Auteurs

Nune Darbinian (N)

Center for Neural Repair and Rehabilitation Shriners Hospitals Pediatric Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.

Gary L Gallia (GL)

Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, MD 21287, USA.

Armine Darbinyan (A)

Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA.

Ekaterina Vadachkoria (E)

Center for Neural Repair and Rehabilitation Shriners Hospitals Pediatric Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.

Nana Merabova (N)

Center for Neural Repair and Rehabilitation Shriners Hospitals Pediatric Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Medical College of Wisconsin-Prevea Health, Green Bay, WI 54304, USA.

Amos Moore (A)

Center for Neural Repair and Rehabilitation Shriners Hospitals Pediatric Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.

Laura Goetzl (L)

Department of Obstetrics & Gynecology, University of Texas, Houston, TX 77030, USA.

Shohreh Amini (S)

Department of Biology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA.

Michael E Selzer (ME)

Center for Neural Repair and Rehabilitation Shriners Hospitals Pediatric Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Departments of Neurology and Neural Sciences, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.

Classifications MeSH