Related Experiment Video

Updated: Jul 7, 2026

Isolation of Chondrocytes and Chondroprogenitors Using Fibronectin Adhesion and Migratory Assay
08:09

Isolation of Chondrocytes and Chondroprogenitors Using Fibronectin Adhesion and Migratory Assay

Published on: October 4, 2024

Focal adhesion kinase/Src suppresses early chondrogenesis: central role of CCN2

Daphne Pala1, Mohit Kapoor, Anita Woods

  • 1Department of Physiology and Pharmacology and Division of Oral Biology, Canadian Institute of Health Research Group in Skeletal Development and Remodeling, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada.

The Journal of Biological Chemistry
|February 16, 2008
PubMed

Insights

Reduced focal adhesion kinase (FAK)/Src signaling is crucial for chondrogenesis, a cartilage development process. Connective tissue growth factor (CCN2) acts downstream of FAK/Src to promote this differentiation.

Area of Science:

  • Cellular biology
  • Developmental biology
  • Biochemistry

Background:

  • Adhesive signaling is integral to cellular differentiation processes, notably chondrogenesis.
  • Focal adhesion kinase (FAK)/Src and CCN2 (connective tissue growth factor) are key regulators of cell adhesion with potential roles in chondrogenesis.

Purpose of the Study:

  • To investigate the specific contributions of FAK/Src signaling and CCN2 to early chondrogenesis.
  • To elucidate the relationship between FAK/Src activity and CCN2 expression during chondrogenic differentiation.

Main Methods:

  • Utilized the micromass culture model, a standard in vitro system for studying chondrogenesis.
  • Employed the FAK/Src inhibitor PP2 to modulate signaling pathways.
  • Assessed gene expression of chondrogenic markers (Ccn2, Agc, Sox6) in wild-type and CCN2-deficient mesenchymal cells.

Main Results:

  • FAK/Src signaling was found to suppress early chondrogenesis, inhibiting the expression of key chondrogenic genes.
  • Inhibition of FAK/Src activity led to increased expression of Ccn2, Agc, and Sox6 in wild-type cells.
  • This upregulation of chondrogenic markers upon FAK/Src inhibition was dependent on the presence of CCN2.

Conclusions:

  • A reduction in FAK/Src signaling is a critical prerequisite for initiating chondrogenic differentiation.
  • CCN2 functions downstream of decreased FAK/Src signaling to actively promote chondrogenesis.
  • These findings highlight a novel regulatory axis involving FAK/Src and CCN2 in cartilage development.

More Related Videos

Visualization of Chondrocyte Intercalation and Directional Proliferation via Zebrabow Clonal Cell Analysis in the Embryonic Meckel’s Cartilage06:40

Visualization of Chondrocyte Intercalation and Directional Proliferation via Zebrabow Clonal Cell Analysis in the Embryonic Meckel’s Cartilage

Published on: October 21, 2015

Related Concept Videos

Cadherins in Tissue Organization01:19

Cadherins in Tissue Organization

The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
Cell Sorting During Development
Cell sorting plays an...
Non-Canonical Wnt Signaling Pathways01:41

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
Non-Canonical Wnt Signaling Pathways01:41

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

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 results in tumor...