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Pertussis toxin inhibits hormonal stimulation of bone resorption in fetal rat limb bones

R F Klein1, R A Nissenson, G J Strewler

  • 1Department of Medicine, Veterans Administration Medical Center, San Francisco, California.

The Journal of Pharmacology and Experimental Therapeutics
|September 1, 1991
PubMed

Insights

This study reveals a G-protein crucial for bone resorption regulation by hormones like parathyroid hormone (PTH). Pertussis toxin inhibits this process, suggesting a common pathway for osteoclast activation.

Area of Science:

  • Endocrinology
  • Cell Biology
  • Biochemistry

Background:

  • Hormonal regulation of bone resorption is not fully understood.
  • Receptors for bone resorbing agents like parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] are on osteoblasts, not osteoclasts, obscuring cellular signaling.
  • The precise cellular mechanisms linking hormonal signals to bone resorption remain unclear.

Purpose of the Study:

  • To investigate the role of GTP-binding proteins (G-proteins) in the cellular signaling pathways controlling bone resorption.
  • To identify potential common signaling pathways involved in osteoclast activation by various bone resorbing agents.

Main Methods:

  • Exposure of fetal rat limb bones to pertussis toxin, a known inhibitor of specific G-proteins.
  • Assessment of bone resorption in response to PTH, 1,25(OH)2D3, and prostaglandin E2.
  • Measurement of alkaline phosphatase activity and cyclic AMP response to PTH.

Main Results:

  • Pertussis toxin significantly inhibited bone resorption induced by PTH, 1,25(OH)2D3, and prostaglandin E2.
  • Pertussis toxin did not inhibit the suppression of alkaline phosphatase activity by PTH or 1,25(OH)2D3.
  • Pertussis toxin potentiated the cyclic AMP response to PTH, indicating a role beyond initial signal transduction.

Conclusions:

  • Data support the existence of a pertussis toxin-sensitive G-protein involved in regulating bone resorption.
  • This G-protein appears to be part of a final common pathway for osteoclast activation, rather than initial signal transduction.
  • Findings suggest a novel mechanism in the hormonal control of bone resorption.

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