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Related Experiment Videos

Osteoclasts are present in gp130-deficient mice

K Kawasaki1, Y H Gao, S Yokose

  • 1Department of Oral Pathology, School of Dentistry, Showa University, Tokyo, Japan.

Endocrinology
|November 5, 1997
PubMed
Summary

gp130 signaling is not essential for osteoclast formation during fetal development. Osteoclast activity in gp130-deficient mice suggests functional redundancy of other bone-resorbing cytokines.

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Area of Science:

  • Biochemistry
  • Developmental Biology
  • Orthopedics

Background:

  • Interleukin (IL)-6 family cytokines (IL-6, IL-11, LIF, OSM) induce osteoclast formation.
  • These cytokines signal through a common transducer, gp130, forming a receptor complex.

Purpose of the Study:

  • Investigate the role of gp130 in osteoclast development.
  • Examine bone tissues in gp130-deficient mice.

Main Methods:

  • Soft x-ray radiography and microfocus x-ray computed tomography.
  • Histological examination of bone tissues.
  • Comparison between gp130-deficient and wild-type newborn mice.

Main Results:

  • Decreased trabecular bone amount in the metaphysial region of tibiae and radii in gp130-deficient mice.

Related Experiment Videos

  • Approximately double the number of osteoclasts in gp130-deficient mice compared to wild-type.
  • No significant differences in osteoblast distribution or osteoid surface.
  • Decreased mineralized bone volume in mandibulae of gp130-deficient mice.

    • Conclusions:

    • Osteoclast formation is not solely dependent on gp130 signaling during fetal development.
    • Increased osteoclastic bone resorption in gp130-deficient mice may involve functional redundancy of other bone-resorbing cytokines.