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The collagen receptor DDR2 regulates proliferation and its elimination leads to dwarfism

J P Labrador1, V Azcoitia, J Tuckermann

  • 1European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany. Labrador@Socrates.Berkeley.edu

EMBO Reports
|May 29, 2001
PubMed

Insights

Discoidin domain receptor 2 (DDR2) deficiency causes dwarfism and impaired wound healing in mice by reducing cell proliferation. DDR2 functions as an extracellular matrix sensor regulating cell growth.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Developmental Biology

Background:

  • Discoidin domain receptor 2 (DDR2) is a receptor tyrosine kinase activated by fibrillar collagens.
  • DDR2 is broadly expressed in postnatal tissues, but its in vivo functions remain largely unknown.

Purpose of the Study:

  • To elucidate the in vivo functions of DDR2.
  • To investigate the role of DDR2 in skeletal development and wound healing.

Main Methods:

  • Generation and analysis of DDR2-deficient (DDR2-/-) mice.
  • Assessment of skeletal phenotypes, including long bone length and chondrocyte proliferation.
  • Evaluation of skin wound healing response in DDR2-/- mice.
  • In vitro proliferation assays using fibroblasts from DDR2-/- mice.

Main Results:

  • DDR2-/- mice exhibit dwarfism and shortened long bones, attributed to reduced chondrocyte proliferation.
  • DDR2 deficiency leads to impaired skin wound healing with a reduced proliferative response.
  • Fibroblasts from DDR2-/- mice show slower proliferation, which is rescued by wild-type DDR2 reintroduction.

Conclusions:

  • DDR2 plays a crucial role in regulating cell proliferation in vivo.
  • DDR2 functions as an extracellular matrix sensor, modulating chondrocyte and fibroblast proliferation.
  • These findings highlight DDR2's importance in skeletal development and tissue repair.

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