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Related Experiment Video

Updated: May 27, 2025

Author Spotlight: An Economic and Efficient Method for Quantitative Evaluation of Bone Microarchitecture in a Murine Osteoporosis Model

Author Spotlight: An Economic and Efficient Method for Quantitative Evaluation of Bone Microarchitecture in a Murine Osteoporosis Model

Published on: September 8, 2023

The microRNA-455 null mouse shows dysregulated bone turnover.

Lingzi Niu¹, Tracey E Swingler¹, Caterina Suelzu²

¹Biomedical Research Centre, School of Biological Sciences, University of East Anglia, Norwich, NR4 7TJ, United Kingdom.

|February 18, 2025

Summary

This summary is machine-generated.

MicroRNA-455 (miR-455) deficiency in mice leads to increased bone length and density in young animals. This bone phenotype is linked to altered osteoblast and osteoclast activity, with FGF18 identified as a key target.

Keywords:

FGF18 bone miR-455 microRNA null mouse

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Last Updated: May 27, 2025

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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Published on: July 3, 2020

Area of Science:

Molecular Biology
Genetics
Bone Biology

Background:

MicroRNAs (miRNAs) play crucial roles in regulating bone mass by influencing osteoblast differentiation and function.
Previous studies have identified specific miRNAs affecting bone metabolism, but the role of miR-455 remained largely uncharacterized.
Our prior work generated a miR-455 knockout mouse model, revealing age-dependent behavioral changes.

Purpose of the Study:

To investigate the impact of miR-455 deficiency on bone development and structure.
To identify the underlying molecular mechanisms, including specific gene targets, responsible for miR-455's effects on bone.
To characterize the bone phenotype in miR-455 null mice across different age points.

Main Methods:

Generation and phenotypic analysis of miR-455 null mice using CRISPR-Cas9 technology.
In vivo assessment of bone length and MicroCT analysis of bone structure (trabecular bone, porosity).
In vitro studies using bone marrow-derived stem cells to evaluate osteogenesis and osteoclastogenesis; gene expression analysis (gain- and loss-of-function) to identify miR-455 targets.

Main Results:

miR-455 null mice exhibited significantly increased long bone and vertebral length at 3 weeks of age, with this difference persisting, though diminishing, up to 1 year.
Increased osteogenesis and decreased osteoclastogenesis/function were observed in miR-455 null mice, correlating with enhanced trabecular bone mass and reduced porosity at 3 weeks.
Fibroblast growth factor 18 (FGF18) was identified and validated as a direct target gene regulated by miR-455.

Conclusions:

miR-455 plays a significant role in regulating bone formation and density, particularly during early development.
The observed bone phenotype in miR-455 null mice is mediated, at least in part, by the regulation of FGF18 expression.
Targeting the miR-455/FGF18 axis presents a potential therapeutic strategy for modulating bone mass.