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Related Experiment Video

Updated: Jun 27, 2025

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

FoxO3 Regulates Mouse Bone Mesenchymal Stem Cell Fate and Bone-Fat Balance During Skeletal Aging.

Wei Yu¹, Min-Ji Tong¹, Guo-Hao Wu¹

¹Department of Orthopedic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.

Stem Cells and Development

|April 25, 2024

Summary

Forkhead box O 3 (FoxO3) controls bone cell differentiation. Restoring FoxO3 levels in aged mice combats osteoporosis and excess marrow fat by balancing bone formation and fat accumulation.

Keywords:

FoxO3 (Forkhead box O 3)adipogenesis aging bone mesenchymal stem cells (BMSCs)osteogenesis osteoporosis

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Last Updated: Jun 27, 2025

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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Area of Science:

Cell Biology
Gerontology
Orthopedics

Background:

Age-related osteoporosis involves imbalanced differentiation of bone mesenchymal stem cells (BMSCs).
Forkhead box O 3 (FoxO3) influences lifespan and cell differentiation.
The role of FoxO3 in age-related bone loss and marrow fat accumulation requires investigation.

Purpose of the Study:

To investigate the role of FoxO3 in regulating age-related bone loss and marrow fat accumulation.
To determine if FoxO3 modulates osteogenic and adipogenic differentiation in BMSCs.

Main Methods:

Detected FoxO3 expression in BMSCs from young and aged mice (in vivo and in vitro).
Modulated FoxO3 expression using adenoviral vectors.
Evaluated bone-fat balance via alizarin red S staining, oil red O staining, qPCR, Western blot, and histology.

Main Results:

FoxO3 expression was downregulated in aged BMSCs, correlating with bone loss and fat accumulation.
Overexpression of FoxO3 in aged mice alleviated bone loss and reduced marrow fat.
FoxO3 suppressed adipogenesis and promoted osteogenesis by downregulating PPAR-γ and Notch signaling.

Conclusions:

FoxO3 is crucial for maintaining the bone-fat balance in BMSCs.
FoxO3 downregulation contributes to age-related osteoporosis and marrow fat accumulation.
FoxO3 represents a potential therapeutic target for preventing age-related osteoporosis.