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Updated: Jun 7, 2025
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Chondrogenic Differentiation Induction of Adipose-derived Stem Cells by Centrifugal Gravity
Published on: February 24, 2017
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Serinc5 Regulates Sequential Chondrocyte Differentiation by Inhibiting Sox9 Function in Pre-Hypertrophic
Kenji Hata1, Kanta Wakamori1,2, Akane Hirakawa-Yamamura1,3
1Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Journal of Cellular Physiology
|November 21, 2024
Summary
Serine incorporator 5 (Serinc5) is a novel marker for pre-hypertrophic chondrocytes, regulating bone growth. It inhibits proliferation and differentiation by targeting Sox9, offering new insights into growth plate development.
Area of Science:
- Cell Biology
- Developmental Biology
- Molecular Biology
Background:
- The growth plate is crucial for longitudinal bone growth, driven by chondrocyte differentiation.
- Pre-hypertrophic chondrocytes are a key transitional cell population, but their molecular regulation is poorly understood.
Purpose of the Study:
- To identify molecular markers and understand the regulatory mechanisms of pre-hypertrophic chondrocytes in the growth plate.
Main Methods:
- Single-cell RNA sequencing (scRNA-seq) of fluorescently labeled growth plate chondrocytes.
- Histological analysis, Chromatin immunoprecipitation sequencing (ChIP-seq), and Assay for Transposase-Accessible Chromatin sequencing (ATAC-seq).
Main Results:
- Serine incorporator 5 (Serinc5) was identified as a specific marker for pre-hypertrophic chondrocytes.
- Serinc5 inhibits chondrocyte proliferation and expression of Col2a1 and Acan by suppressing Sox9 transcriptional activity.
- An active enhancer for Serinc5 was found in intron 1, with chromatin status increasing during differentiation.
Conclusions:
- Serinc5 plays a critical role in regulating chondrocyte differentiation from proliferation to hypertrophy by inhibiting Sox9 in pre-hypertrophic chondrocytes.
- These findings provide novel insights into the molecular mechanisms governing growth plate development and endochondral ossification.
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