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Expression of SHOX in human fetal and childhood growth plate

C J F Munns1, H R Haase, L M Crowther

  • 1Endocrine Research Unit, Royal Children's Hospital Foundation Research Centre, and Department of Paediatrics and Child Health, University of Queensland, Royal Children's Hospital, Brisbane QLD 4029, Australia.

The Journal of Clinical Endocrinology and Metabolism
|August 5, 2004
PubMed

Insights

Short stature and skeletal deformities, like Leri Weil syndrome, are linked to SHOX gene mutations. This study found SHOX protein and mRNA present in normal and Leri Weil growth plates, suggesting its role in chondrocyte function.

Area of Science:

  • Genetics
  • Developmental Biology
  • Orthopedics

Background:

  • Abnormalities in the growth plate can cause short stature and skeletal deformities.
  • Leri Weil syndrome is associated with mutations or deletions in the SHOX gene, located on the pseudoautosomal region of sex chromosomes.

Purpose of the Study:

  • To investigate the expression patterns of SHOX protein and mRNA in human fetal and childhood growth plates.
  • To compare SHOX expression in normal growth plates versus those affected by Leri Weil syndrome.

Main Methods:

  • Immunohistochemistry was used to detect SHOX protein in fetal and childhood growth plates.
  • In situ hybridization was employed to analyze SHOX mRNA expression in childhood normal and Leri Weil growth plates.

Main Results:

  • SHOX protein was detected in all zones (reserve, proliferative, hypertrophic) of fetal and childhood growth plates, including those from Leri Weil syndrome patients.
  • SHOX mRNA was expressed throughout the growth plate in childhood samples.
  • No significant differences in SHOX protein or mRNA expression patterns were observed between control and Leri Weil growth plates.

Conclusions:

  • The study suggests that SHOX protein and mRNA are present in growth plates, indicating a role in chondrocyte function.
  • The findings do not reveal altered expression patterns of SHOX in Leri Weil syndrome, implying potential regulatory or functional differences beyond expression levels.

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