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Chondrocytes form a temporary cartilaginous model by dividing and secreting a thick gel-like extracellular matrix. Once the chondrocytes undergo programmed cell death, osteoblasts enter the site of the cartilaginous model. The process of replacing the temporary cartilaginous model with bone in an ordered manner is called endochondral ossification. In endochondral ossification, not all of the cartilage is replaced by bone tissue. Some cartilage that performs a protective and supportive function...
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Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...
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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...
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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Updated: Sep 12, 2025

Laser Capture Microdissection of Mouse Embryonic Cartilage and Bone for Gene Expression Analysis
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Fibroblast Growth Factor 19 Disrupts Cartilage Development Via the FGFR4/β-catenin Axis.

Hao Chen1, Yujia Cui1, Jiazhou Li1

  • 1State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.

International Journal of Biological Sciences
|August 6, 2025
PubMed
Summary

Fibroblast growth factor 19 (FGF19) impairs cartilage development by inhibiting chondrocyte maturation and growth plate thickness. This occurs through the FGFR4/β-catenin pathway, affecting skeletal growth.

Keywords:
Wnt/β-Cateninchondrogenesisfibroblast growth factor 19growth plate

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Area of Science:

  • Skeletal Biology
  • Endocrinology
  • Developmental Biology

Background:

  • Fibroblast growth factor 19 (FGF19) is implicated in skeletal metabolic disorders.
  • The specific role of FGF19 in cartilage development remains unclear.

Purpose of the Study:

  • To investigate the influence of FGF19 on cartilage development and chondrogenesis.
  • To elucidate the molecular mechanisms underlying FGF19's effects on growth plate chondrocytes.

Main Methods:

  • Utilized an ex vivo metatarsal organ model for neonatal cartilage.
  • Employed an adeno-associated virus (AAV)-FGF19 overexpression model in adolescent growth plates.
  • Assessed chondrocyte differentiation, maturation, and proliferation markers.

Main Results:

  • FGF19 impaired chondrocyte maturation in neonatal models and reduced growth plate thickness in adolescent models.
  • FGF19 decreased mesenchymal stem cell chondrogenic differentiation and chondrocyte maturation by downregulating Wnt/β-catenin signaling.
  • FGF19 signaling, via FGFR4 and β-klotho (KLB), activated Wnt antagonists (SFRP1, WIF1, DKK2), inhibiting chondrocyte proliferation and cartilage growth.

Conclusions:

  • FGF19 inhibits cartilage development and growth plate chondrogenesis through the FGFR4/β-catenin axis.
  • This study provides novel insights into the role of FGF19 in endochondral ossification and skeletal development.