ArticleEndocrinology2012
Conditional inactivation of noggin in the postnatal skeleton causes osteopenia.
Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 35 citations in OpenAlex.
- Noggin promotes osteogenesis in human adipose-derived mesenchymal stem cells via FGFR2/Src/Akt and ERK signaling pathway.Scientific reports · 2024Article
- The roles and regulatory mechanisms of TGF-β and BMP signaling in bone and cartilage development, homeostasis and disease.Cell research · 2024Review
- Wnt/β-catenin signalling: function, biological mechanisms, and therapeutic opportunities.Signal transduction and targeted therapy · 2022Review
- Skeleton-vasculature chain reaction: a novel insight into the mystery of homeostasis.Bone research · 2021Review
- Circulating noggin levels following treatment with denosumab or teriparatide in postmenopausal women with low bone mass.Journal of musculoskeletal & neuronal interactions · 2019Observational
- Novel protective and risk loci in hip dysplasia in German Shepherds.PLoS genetics · 2019Article
- Expression of Noggin and Gremlin1 and its implications in fine-tuning BMP activities in mouse cartilage tissues.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2017Article
- Cortical-Bone Fragility--Insights from sFRP4 Deficiency in Pyle's Disease.The New England journal of medicine · 2016Article
- Regulation of tissue morphogenesis by endothelial cell-derived signals.Trends in cell biology · 2015Review
- Systemic injection of CK2.3, a novel peptide acting downstream of bone morphogenetic protein receptor BMPRIa, leads to increased trabecular bone mass.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2015Article
- Dynamics and cellular localization of Bmp2, Bmp4, and Noggin transcription in the postnatal mouse skeleton.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2015Article
- The effect of noggin interference in a rabbit posterolateral spinal fusion model.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2014Article
- Article
- BMP signaling in mesenchymal stem cell differentiation and bone formation.Journal of biomedical science and engineering · 2013Article
- WNT signaling in bone homeostasis and disease: from human mutations to treatments.Nature medicine · 2013Review
- A soluble bone morphogenetic protein type IA receptor increases bone mass and bone strength.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
Noggin is an antagonist of bone morphogenetic proteins (BMP), and its overexpression causes suppressed osteoblastogenesis and osteopenia. Global inactivation of Noggin results in severe developmental defects and prenatal lethality, but the consequences of the conditional inactivation of Noggin on the postnatal skeleton are not known. To study the function of noggin in osteoblasts, we generated tissue-specific null Noggin mice by mating Noggin conditional mice, where the Noggin allele is flanked by loxP sequences, with mice expressing the Cre recombinase under the control of the osteocalcin promoter (Oc-Cre). Noggin conditional null mice exhibited decreased weight, shortened femoral length, and generalized osteopenia. Bone histomorphometric and microarchitectural analyses of distal femurs revealed decreased bone volume due to a reduced number of trabeculae in 1- and 3-month-old Noggin conditional null mice. Vertebral microarchitecture confirmed the osteopenia observed in Noggin conditional null mice. Osteoclast number was increased in 1-month-old male Noggin conditional null mice, and bone formation was increased in 3-month-old mice, but female mice did not exhibit increased bone remodeling. In conclusion, Noggin inactivation causes osteopenia, suggesting that BMP in excess have a detrimental effect on bone or that noggin has a BMP-independent role in skeletal homeostasis.
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What OpenQuestion holds
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.