Identification of Genes and microRNAs Associated with Midfacial Hypoplasia in Mice

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.

Authors

Institutions

Publication Details

Journal
Cells
Published
2026-03-03
DOI
https://doi.org/10.3390/cells15050453
Primary Topic
Cleft Lip and Palate Research
Type
article
Field-Weighted Citation Impact
0.00

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Identification of Genes and microRNAs Associated with Midfacial Hypoplasia in Mice

Chihiro Iwaya, A. SUZUKI, 岩田 純一, Ashley Jung et al.
Cells
Cleft Lip and Palate Research
article

Identification of Genes and microRNAs Associated with Midfacial Hypoplasia in Mice

Chihiro Iwaya, A. SUZUKI, 岩田 純一, Ashley Jung, Ashley Huang
article en

Abstract

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.

CellsVol. 15(5)
University of Michigan (US), The University of Texas Health Science Center at Houston (US)
University of Michigan, National Institutes of Health
Openalex Percentile: Top 36%
Cleft Lip and Palate Research
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.

Identification of Genes and microRNAs Associated with Midfacial Hypoplasia in Mice — Chihiro Iwaya, A. SUZUKI, et al. · Cells (2026) | TGRS Research Map | TGRS