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Ectopic SOX9 mediates extracellular matrix deposition characteristic of organ fibrosis

Karen Piper Hanley1, Fiona Oakley, Sarah Sugden

  • 1Centre for Human Development, Stem Cells & Regeneration. k.piper@soton.ac.uk

The Journal of Biological Chemistry
|February 26, 2008
PubMed

Insights

Ectopic SOX9 expression, induced by histone deacetylase inhibitors, drives disease-associated gene expression. This SOX9 role in fibrosis suggests new therapeutic targets for liver disease.

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Pathology

Background:

  • SOX9 is crucial for organ development.
  • Aberrant SOX9 expression is linked to disease.
  • Histone deacetylase inhibitors (HDACi) are used in cancer therapy.

Purpose of the Study:

  • Investigate SOX9 regulation by HDACi.
  • Determine SOX9's role in disease pathology, specifically fibrosis.

Main Methods:

  • Utilized histone deacetylase inhibitors to induce SOX9 expression.
  • Examined SOX9's effect on gene expression in hepatocytes and fibrogenic cells.
  • Analyzed SOX9's role in extracellular matrix (ECM) deposition.

Main Results:

  • HDACi induced SOX9 expression in cells lacking it, like hepatocytes.
  • Ectopic SOX9 triggered chondrogenic gene expression (COL2A1, COMP1) in fetal hepatocytes.
  • SOX9 drove type 1 collagen expression in activated adult liver fibrogenic cells, a key fibrotic ECM component.

Conclusions:

  • SOX9 expression is regulated by enhanced nuclear factor Y (NF-Y) recruitment to the SOX9 promoter by HDACi.
  • SOX9 contributes to fibrosis by regulating ECM deposition.
  • SOX9 has a role in disease pathology beyond normal development.

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