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Bone formation in the context of growth retardation induced by hIGFBP-1 overexpression in transgenic mice

N Ben Lagha1, P Menuelle, D Seurin

  • 1Laboratoire de Biologie-Orofaciale et Pathologie, INSERM EMI U-0110, Université Paris 7, IFR 58, Institut Biomédical des Cordeliers, Esc. E, 2è ét., 15-21 rue de l'Ecole de Médecine, 75270 Paris, France. Pierrette.Menuelle@bhdc.jussieu.fr

Connective Tissue Research
|December 20, 2002
PubMed

Insights

Overexpression of human insulin-like growth factor binding protein 1 (hIGFBP-1) in mice caused growth retardation and delayed bone mineralization, mirroring human intrauterine growth retardation (hIUGR) effects.

Area of Science:

  • Endocrinology
  • Developmental Biology
  • Skeletal Biology

Background:

  • Human intrauterine growth retardation (hIUGR) is linked to increased insulin-like growth factor binding protein 1 (IGFBP-1) levels.
  • Children with hIUGR often exhibit delayed bone mineralization.

Purpose of the Study:

  • To investigate the role of IGFBP-1 in growth and bone mineralization using a mouse model.
  • To determine if IGFBP-1 overexpression can induce growth retardation and mineralization defects.

Main Methods:

  • Generated transgenic mice overexpressing human IGFBP-1 (hIGFBP-1) in the liver.
  • Assessed skeletal development and mineralization using Alcian blue and alizarin red S staining.
  • Analyzed bone density via microradiography.

Main Results:

  • Transgenic mice exhibited severe postnatal growth retardation.
  • Significant mineralization defects were observed in the skull, axial, and appendicular skeleton.
  • Reduced bone density was confirmed in affected skeletal regions.

Conclusions:

  • Hepatospecific overexpression of hIGFBP-1 leads to early postnatal growth retardation and impaired bone mineralization in mice.
  • These findings highlight the critical involvement of the IGF/IGFBP system, particularly IGFBP-1, in the biomineralization process.

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