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Enhanced cortical bone expansion in Lgals3-deficient mice during aging.

PMID: 30886760 (view PubMed database entry)
DOI: 10.1038/s41413-017-0003-6 (read at publisher's website )
PMCID: PMC6416267 (free full text version available)

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Kevin A Maupin, Kevin Weaver, Alexis Bergsma, Cheryl Christie, Zhendong A Zhong, Tao Yang, Bart O Williams,

Imbalances between bone formation and bone resorption, which can occur due to aging or sex hormone deprivation, result in decreased bone mass and an increased risk of fracture. Previous studies have suggested that the β-galactoside binding lectin, galectin-3, is involved in bone remodeling. We compared bone parameters of mice having null alleles of the galectin-3 gene (Lgals3-KO) with those of their wild-type littermates. Lgals3 deficiency increased cortical bone expansion at 36 weeks (wk) and preserved or enhanced bone mass in both male and female mutant mice. In addition, female Lgals3-KO mice were protected from age-related loss of trabecular bone. Histomorphometry and ex vivo primary cell differentiation assays showed increased osteoblastogenesis with little-to-no effect on osteoclastogenesis, suggesting the increased bone mass phenotype is primarily due to increased anabolism. Our study identifies galectin-3 as a negative regulator of bone formation and suggests that disruption of galectin-3 may be useful in preventing bone loss during aging.

Bone Res (Bone research)
[2018, 6:7]

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