Faculty, Staff and Student Publications
Language
English
Publication Date
5-1-2022
Journal
Development
DOI
10.1242/dev.200476
PMID
35420127
PMCID
PMC9148563
PubMedCentral® Posted Date
5-3-2022
PubMedCentral® Full Text Version
Post-print
Abstract
The etiology of cleft lip with or without cleft palate (CL/P), a common congenital birth defect, is complex, with genetic and epigenetic, as well as environmental, contributing factors. Recent studies suggest that fetal development is affected by maternal conditions through microRNAs (miRNAs), a group of short noncoding RNAs. Here, we show that miR-129-5p and miR-340-5p suppress cell proliferation in both primary mouse embryonic palatal mesenchymal cells and O9-1 cells, a neural crest cell line, through the regulation of Sox5 and Trp53 by miR-129-5p, and the regulation of Chd7, Fign and Tgfbr1 by miR-340-5p. Notably, miR-340-5p, but not miR-129-5p, was upregulated following all-trans retinoic acid (atRA; tretinoin) administration, and a miR-340-5p inhibitor rescued the cleft palate (CP) phenotype in 47% of atRA-induced CP mice. We have previously reported that a miR-124-3p inhibitor can also partially rescue the CP phenotype in atRA-induced CP mouse model. In this study, we found that a cocktail of miR-124-3p and miR-340-5p inhibitors rescued atRA-induced CP with almost complete penetrance. Taken together, our results suggest that normalization of pathological miRNA expression can be a preventive intervention for CP.
Keywords
Animals, Cell Proliferation, Cleft Lip, Cleft Palate, Mice, MicroRNAs, Tretinoin
Published Open-Access
yes
Recommended Citation
, "Suppression of microRNA 124–3p and microRNA 340–5p Ameliorates Retinoic Acid-Induced Cleft Palate in Mice" (2022). Faculty, Staff and Student Publications. 83.
https://digitalcommons.library.tmc.edu/uthdb_docs/83