# Identification of Genes and microRNAs Associated with Midfacial Hypoplasia in Mice

## TL;DR

This study identifies genes and microRNAs linked to midfacial hypoplasia in mice, offering insights into its development and potential treatments.

## Contribution

The study identifies specific microRNAs and genes involved in midfacial hypoplasia regulation in mice.

## Key findings

- 224 genes associated with midfacial malformations in mice were identified.
- Eight microRNAs, including miR-129-5p and miR-381-3p, were predicted to regulate these genes.
- Overexpression of top microRNAs inhibited cell proliferation and osteogenesis in nasal process mesenchymal cells.

## Abstract

What are the main findings?
Genes linked to midfacial hypoplasia have been identified in mouse models.MicroRNAs specific to midfacial hypoplasia have been identified in mice.

Genes linked to midfacial hypoplasia have been identified in mouse models.

MicroRNAs specific to midfacial hypoplasia have been identified in mice.

What are the implications of the main findings?
Support the development of strategies to prevent and treat midfacial hypoplasia.Improve understanding of midfacial hypoplasia mechanisms.

Support the development of strategies to prevent and treat midfacial hypoplasia.

Improve understanding of midfacial hypoplasia mechanisms.

Midfacial hypoplasia is a developmental defect caused by insufficient growth of the nasal placodes and maxillary prominences. While genetic studies in mice have identified key genes involved in midfacial development, the regulation of these genes during craniofacial development remains poorly understood. In this study, we demonstrate that microRNAs, short non-coding RNAs, play a crucial role in regulating genes involved in midfacial development. We identified 224 genes associated with midfacial malformations in mice. Through bioinformatics analyses, we predicted that several microRNAs, specifically miR-129-5p, miR-381-3p, miR-124-3p, miR-136-5p, miR-448-3p, miR-374, miR-96, and miR-882, could regulate the expression of these genes. Among these, we experimentally focused on the top four candidate microRNAs: miR-129-5p, miR-381-3p, miR-124-3p, and miR-136-5p. Our findings revealed that the overexpression of these microRNAs inhibited cell proliferation and osteogenesis in nasal process mesenchymal cells. These microRNAs regulated genes associated with midfacial malformations in a dose-dependent manner. Taken together, our results emphasize the significance of pathogenic microRNA–gene networks in the cause of midfacial malformations.