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Skeletal abnormalities in mice lacking extracellular matrix proteins, thrombospondin-1, thrombospondin-3,

Karen L Posey1, Kurt Hankenson, Alka C Veerisetty

  • 1Department of Pediatrics, University of Texas Medical School, 6431 Fannin, Houston, TX 77030, USA.

The American Journal of Pathology
|May 10, 2008
PubMed

Insights

Thrombospondin-5 (TSP5) and type IX collagen (Col9) are crucial for skeletal growth. Combined deficiencies in TSP3, TSP5, and Col9 significantly reduce limb length, impacting growth plate organization.

Area of Science:

  • Biochemistry
  • Genetics
  • Skeletal Biology

Background:

  • Thrombospondin-5 (TSP5) is an extracellular matrix glycoprotein implicated in skeletal dysplasias.
  • Mutations in TSP5 cause pseudoachondroplasia and multiple epiphyseal dysplasia, characterized by growth plate abnormalities.
  • Previous studies on TSP5 function in the growth plate are limited, with knockout mice showing no overt skeletal defects.

Purpose of the Study:

  • To elucidate the specific roles of Thrombospondin-1 (TSP1), TSP3, TSP5, and type IX collagen (Col9) in growth plate organization and skeletal development.
  • To investigate the functional redundancy and combinatorial effects of these extracellular matrix proteins.

Main Methods:

  • Histomorphometric analysis of various knockout mouse strains, including single and combinatorial knockouts for TSP1, TSP3, TSP5, and Col9.
  • Evaluation of growth plate organization, skeletal growth, and limb length in mutant mice.

Main Results:

  • Single knockout mice exhibited some growth plate alterations but only mild skeletal growth disturbances.
  • Combinatorial knockout of TSP3, TSP5, and Col9 led to significant growth plate disorganization.
  • TSP3/5/Col9 knockout mice showed a 20% reduction in limb length, indicating a severe impact on skeletal growth.

Conclusions:

  • Type IX collagen (Col9) may play a role in regulating growth plate width.
  • TSP3, TSP5, and Col9 collectively contribute to maintaining growth plate organization.
  • TSP1 might be involved in regulating growth plate closure, particularly in the absence of other extracellular proteins.

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