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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
Published on: July 3, 2020
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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model.
Yiling Yang1, Qianye Chen2, Siru Zhou1
1Center of Craniofacial Orthodontics, Department of Oral and Cranio-maxillofacial Science, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology, National Clinical Research center of Stomatology.
Journal of Visualized Experiments : Jove
|July 28, 2020
Summary
Signal transducer and activator of transcription 3 (STAT3) is crucial for osteoclast activity. Deleting STAT3 in osteoclasts led to increased bone mass, highlighting its role in bone metabolism.
Area of Science:
- Bone biology and skeletal physiology.
- Transgenic mouse models in biomedical research.
- Osteoclast differentiation and function.
Background:
- Osteoporosis pathogenesis involves dysregulated osteoclast activity.
- Signal transducer and activator of transcription 3 (STAT3) is implicated in bone homeostasis.
- The specific role of STAT3 in osteoclasts in vivo requires elucidation.
Purpose of the Study:
- To investigate the in vivo role of STAT3 in osteoclast differentiation and bone metabolism.
- To generate and analyze an osteoclast-specific Stat3 deletion mouse model (Stat3fl/fl; Ctsk-Cre).
Main Methods:
- Generation of a conditional knockout mouse model using Cathepsin K (Ctsk)-Cre and Stat3fl/fl mice.
- Skeletal phenotyping using micro-computed tomography (Micro-CT) and 3D reconstruction.
- Histological analysis including Hematoxylin and Eosin (H&E) staining, calcein and alizarin red double staining, and tartrate-resistant acid phosphatase (TRAP) staining.
Main Results:
- Conditional knockout mice exhibited increased bone mass compared to controls.
- Micro-CT analysis revealed significant alterations in bone structure.
- Histological analyses provided insights into bone metabolism and osteoclast activity.
Conclusions:
- STAT3 plays a critical role in regulating osteoclast differentiation and activity in vivo.
- Targeting STAT3 in osteoclasts may offer a therapeutic strategy for osteoporosis.
- This study provides a foundation for further research into STAT3-mediated bone metabolism.

