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Versican A-subdomain is required for its adequate function in dermal development.

Sonoko Hatano1, Naoko Nagai1, Nobuo Sugiura1

  • 1a Institute for Molecular Science of Medicine, Aichi Medical University , Aichi , Japan.

Connective Tissue Research
|May 11, 2017
PubMed
Summary
This summary is machine-generated.

The A-subdomain of versican is crucial for its dermal expression and extracellular matrix (ECM) accumulation. Its absence impairs ECM structure, collagen biosynthesis, and TGFβ signaling, leading to neonatal death in mutant mice.

Keywords:
CollagenTGFβextracellular matrixhyaluronanversican

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Area of Science:

  • Dermatology
  • Molecular Biology
  • Developmental Biology

Background:

  • Versican is a key extracellular matrix (ECM) proteoglycan regulating cell behavior.
  • Its role in dermal development and ECM formation is not fully understood.

Purpose of the Study:

  • To investigate the function of versican in dermal development using a mouse model with a deleted A-subdomain.
  • To elucidate the impact of impaired versican function on ECM structure, cell density, and signaling pathways.

Main Methods:

  • Utilized VcanΔ3/Δ3 mutant mice lacking the versican A-subdomain.
  • Analyzed dermal ECM structure, cell density, collagen deposition and biosynthesis.
  • Assessed transforming growth factor β (TGFβ) signaling pathway activity and gene expression via microarray analysis.

Main Results:

  • Mutant versican exhibited reduced hyaluronan binding and ECM accumulation.
  • VcanΔ3/Δ3 mice showed decreased versican expression, impaired dermal ECM, reduced cell density, and decreased collagen biosynthesis.
  • TGFβ signaling was down-regulated in mutant fibroblasts, with reduced TGFβ storage in the ECM and decreased expression of Egr2 and Egr4 transcription factors.

Conclusions:

  • The versican A-subdomain is essential for proper versican expression and ECM formation in the dermis.
  • Versican plays a critical role in regulating ECM structure, collagen biosynthesis, and TGFβ signaling during dermal development.
  • Impaired versican function leads to severe developmental defects and neonatal lethality.