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

Robert Klein, R. A. Nissenson, G. J. Strewler

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

The cellular basis for hormonal control of bone resorption is poorly understood. As the identifiable receptors for bone resorbing agents such as parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] are located on osteoblasts rather than osteoclasts, the nature of cellular signaling is obscure. Here it is reported that exposure of fetal rat limb bones to pertussis toxin, a bacterial protein that inhibits certain GTP binding proteins (G-proteins) involved in signal transduction, markedly inhibits bone resorption elicited by PTH, 1,25(OH)2D3 and prostaglandin E2. Pertussis toxin does not block the inhibition of alkaline phosphatase activity by PTH or 1,25(OH)2D3, and it potentiates the cyclic AMP response to PTH. These data support the existence of a pertussis toxin-sensitive G-protein that participates in regulation of bone resorption. The putative G-protein is apparently not involved in the initial transduction of hormonal signals, but it may be part of a final common pathway through which the osteolast is activated by agents with widely divergent initial actions.

Original languageEnglish (US)
Pages (from-to)877-881
Number of pages5
JournalJournal of Pharmacology and Experimental Therapeutics
Volume258
Issue number3
StatePublished - 1991

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Pertussis Toxin
Bone Resorption
Parathyroid Hormone
Extremities
GTP-Binding Proteins
Bone and Bones
Signal Transduction
Bacterial Proteins
Calcitriol
Osteoclasts
Osteoblasts
Dinoprostone
Cyclic AMP
Alkaline Phosphatase

ASJC Scopus subject areas

  • Pharmacology

Cite this

Pertussis toxin inhibits hormonal stimulation of bone resorption in fetal rat limb bones. / Klein, Robert; Nissenson, R. A.; Strewler, G. J.

In: Journal of Pharmacology and Experimental Therapeutics, Vol. 258, No. 3, 1991, p. 877-881.

Research output: Contribution to journalArticle

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