AI Article Synopsis
- The study explored how PTH and PTHrP affect the bones of mice lacking PTH, revealing that both mutant types had similar hypoparathyroid issues.
- PTH(-/-) mice showed increased trabecular bone volume due to reduced bone breakdown, while those with reduced PTHrP levels lost bone mass by hindering new bone cell formation.
- The findings highlight PTHrP's important role in bone development and suggest its potential use as a treatment to promote bone growth.
Article Abstract
We investigated the relative contributions of PTH and PTHrP to the skeletal phenotype of mice deficient in PTH (PTH(-/-)). PTH(-/-) mice and PTH(-/-) mice lacking one allele encoding PTHrP (PTH(-/-)PTHrP(+/-)) were compared. Both mutants displayed similar biochemical abnormalities of hypoparathyroidism, but skeletal PTHrP mRNA and protein were decreased in PTH(-/-)PTHrP(+/ -) mice. PTH(-/-) mice had increased trabecular bone volume with diminished bone turnover. PTHrP haploinsufficiency reduced trabecular bone of the PTH(-/-) mice to levels below those in wild-type animals by decreasing osteoprogenitor cell recruitment, enhancing osteoblast apoptosis, and diminishing bone formation. The results show that the increased trabecular bone volume in PTH-deficient mice is due to diminished PTH-induced osteoclastic bone resorption and persistent PTHrP-stimulated osteoblastic bone formation. They also illustrate the changing role of PTHrP during bone development, demonstrate its bone- forming function in the postnatal state, and support its pharmacological potential as an anabolic agent.
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| http://dx.doi.org/10.1210/en.2003-1695 | DOI Listing |
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