ArticleOsteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA2011
Deleting Rac1 improves vertebral bone quality and resistance to fracture in a murine ovariectomy model.
Article in Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Rgnef regulates bone mass through the activation of RhoA and Rac1.Experimental & molecular medicine · 2026Article
- Potential therapeutic role of spermine via Rac1 in osteoporosis: Insights from zebrafish and mice.Zoological research · 2024Article
- RhoA promotes osteoclastogenesis and regulates bone remodeling through mTOR-NFATc1 signaling.Molecular medicine (Cambridge, Mass.) · 2023Article
- Bioinformatics analysis identification ofExperimental and therapeutic medicine · 2022Article
- Osteoclast fusion and bone loss are restricted by interferon inducible guanylate binding proteins.Nature communications · 2021Article
- Identification of key gene networks associated with fracture healing using αSMA‑labeled progenitor cells.Molecular medicine reports · 2018Article
- Modulation of osteoclast differentiation and bone resorption by Rho GTPases.Small GTPases · 2014Review
- Differential effects of PPAR-{gamma} activation versus chemical or genetic reduction of DPP-4 activity on bone quality in mice.Endocrinology · 2011Article
- The Roles of Small GTPases in Osteoclast Biology.Orthopedic & muscular system : current researchArticle
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4 authors at 2 institutions in 1 country.
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Abstract
summaryThe roles of Rac1 and Rac2 in regulating osteoclast-mediated bone quality in postmenopausal osteoporosis were evaluated using an ovariectomized murine model. Animals' bone composition and architecture were evaluated. Our results demonstrate that the deletion of Rac1 increases vertebral bone quality compared to wild-type bones in an ovariectomized model.
introductionTo determine the roles of the Rho family small GTPases Rac1 and Rac2 in regulating osteoclast-mediated bone quality in a model of postmenopausal osteoporosis.
methodsTwelve-month-old female mice from three genotypes-wild type (WT), Rac1 null (LysM.Rac1 KO), and Rac2 null (Rac2KO)--were studied in control and ovariectomized groups (mice previously ovariectomized at 4 months of age). Animals were sacrificed at 12 months of age, and the femora and vertebrae were harvested for mechanical testing, bone densitometry, micro-computed tomography, and histomorphometric analyses to evaluate bone mineralization and architecture. The results were compared between groups using ANOVA and LSD post-hoc tests.
resultsWe observed that LysM.Rac1 KO mice showed higher vertebral bone mineral density compared to WT in both control and ovariectomized groups. Consistent with this finding, LysM.Rac1 KO vertebrae showed increased resistance to fracture and increased trabecular connectivity compared to WT in both groups. Micro-CT analysis revealed that Rac2KO ovariectomized vertebrae have more trabecular bone compared to WT and LysM.Rac1 KO, but this did not translate into increased fracture resistance.
conclusionOur results demonstrate that the deletion of Rac1 increases vertebral bone quality compared to WT bones in a postmenopausal osteoporosis model.
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