ArticleBone2011
Primary osteopathy of vertebrae in a neurofibromatosis type 1 murine model.
Article in Bone, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 38 citations in OpenAlex.
- Pharmacological inhibition of RAS pathway alleviates spine deformity in a mouse model of neurofibromatosis type 1.Bone research · 2025Article
- Generation of heterozygous and homozygous NF1 lines from human-induced pluripotent stem cells using CRISPR/Cas9 to investigate bone defects associated with neurofibromatosis type 1.Frontiers in cell and developmental biology · 2024Article
- Review
- Natural History of Scoliosis in Children with NF1: An Observation Study.Healthcare (Basel, Switzerland) · 2021Article
- Ankle loading ameliorates bone loss from breast cancer-associated bone metastasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- The involvement of endoplasmic reticulum formation and protein synthesis efficiency in VCP- and ATL1-related neurological disorders.Journal of biomedical science · 2018Review
- RASopathies: unraveling mechanisms with animal models.Disease models & mechanisms · 2015Review
- Article
- Hyperactive transforming growth factor-β1 signaling potentiates skeletal defects in a neurofibromatosis type 1 mouse model.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2013Article
- Optimizing biologically targeted clinical trials for neurofibromatosis.Expert opinion on investigational drugs · 2013Review
- Height assessments in children with neurofibromatosis type 1.Journal of child neurology · 2013Article
- Article
- Valosin-containing protein and neurofibromin interact to regulate dendritic spine density.The Journal of clinical investigation · 2011Article
- Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Neurofibromatosis type 1 (NF1) is a common autosomal dominant genetic disorder caused by mutation of the NF1 tumor suppressor gene. Spinal deformities are common skeletal manifestations in patients with NF1. To date, the mechanism of vertebral abnormalities remains unclear because of the lack of appropriate animal models for the skeletal manifestations of NF1. In the present study, we report a novel murine NF1 model, Nf1(flox/-);Col2.3Cre(+) mice. These mice display short vertebral segments. In addition, a significant reduction in cortical and trabecular bone mass of the vertebrae was observed in Nf1(flox/-);Col2.3Cre(+) mice as measured by dual-energy X-ray absorptiometry (DEXA) and peripheral quantitative computed tomography (pQCT). Peak stress and peak load were also significantly reduced in Nf1(flox/-);Col2.3Cre(+) mice as compared to controls. Furthermore, the lumbar vertebrae showed enlargement of the inter-vertebral canal, a characteristic feature of lumbar vertebrae in NF1 patients. Finally, histologic analysis demonstrated increased numbers of osteoclasts and decreased numbers of osteoblasts in the vertebrae of Nf1(flox/-);Col2.3Cre(+) mice in comparison to controls. In summary, Nf1(flox/-);Col2.3Cre(+) mice demonstrate multiple structural and functional abnormalities in the lumbar vertebrae which recapitulate the dystrophic vertebral changes in NF1 patients. This novel murine model provides a platform to understand the cellular and molecular mechanisms underlying the pathogenesis of spinal deficits in NF1 patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.