ArticleBone2015
Osteoblast function and bone histomorphometry in a murine model of Rett syndrome.
Article in Bone, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Increased Osteoclast Activity Contributes to Bone Resorption and Osteopenia in a Rett Syndrome Mouse Model.Cells · 2026Article
- MECP2 Insufficiency Attenuates RUNX2-Dependent Osteoblast Differentiation via miR-126-3p/DKK1-Mediated Canonical Wnt Signaling Inhibition in Rett Syndrome.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Disrupted Vitamin D Signaling and Metabolism in Neurodevelopmental and Neurodegenerative Disorders.ASN neuro · 2026Review
- Bone health and bisphosphonate treatment in females with Rett syndrome in a national center.Pediatric research · 2025Article
- Mild antiresorptive activity of an anti-vascular endothelial growth factor A antibody and sunitinib in a rat model of bone resorption.Bone reports · 2025Article
- The Management of Bone Defects in Rett Syndrome.Calcified tissue international · 2025Review
- Bone Fracture in Rett Syndrome: Mechanisms and Prevention Strategies.Children (Basel, Switzerland) · 2023Review
- MiR-422a promotes adipogenesis via MeCP2 downregulation in human bone marrow mesenchymal stem cells.Cellular and molecular life sciences : CMLS · 2023Article
- Altered Bone Status in Rett Syndrome.Life (Basel, Switzerland) · 2021Review
- Rett syndrome: think outside the (skull) box.Faculty reviews · 2021Review
- Effects of Early Life Stress on Bone Homeostasis in Mice and Humans.International journal of molecular sciences · 2020Observational
- Oral health experiences of individuals with Rett syndrome: a retrospective study.BMC oral health · 2018Article
- Clinical and biological progress over 50 years in Rett syndrome.Nature reviews. Neurology · 2017Review
- Exclusive expression of MeCP2 in the nervous system distinguishes between brain and peripheral Rett syndrome-like phenotypes.Human molecular genetics · 2016Article
- Bone microarchitecture in Rett syndrome and treatment with teriparatide: a case report.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Rett syndrome (RTT) is an X-linked neurodevelopmental disorder due to mutations affecting the neural transcription factor MeCP2. Approximately 50% of affected females have decreased bone mass. We studied osteoblast function using a murine model of RTT. Female heterozygote (HET) and male Mecp2-null mice were compared to wild type (WT) mice. Micro-CT of tibia from 5 week-old Mecp2-null mice showed significant alterations in trabecular bone including reductions in bone volume fraction (-29%), number (-19%), thickness (-9%) and connectivity density (-32%), and increases in trabecular separation (+28%) compared to WT. We also found significant reductions in cortical bone thickness (-18%) and in polar moment of inertia (-45%). In contrast, cortical and trabecular bone from 8 week-old WT and HET female mice were not significantly different. However, mineral apposition rate, mineralizing surface and bone formation rate/bone surface were each decreased in HET and Mecp2-null mice compared to WT mice. Histomorphometric analysis of femurs showed decreased numbers of osteoblasts but similar numbers of osteoclasts compared to WT, altered osteoblast morphology and decreased tissue synthesis of alkaline phosphatase in Mecp2-null and HET mice. Osteoblasts cultured from Mecp2-null mice, which unlike WT osteoblasts did not express MeCP2, had increased growth rates, but reductions in mRNA expression of type I collagen, Runx2 and Osterix compared to WT osteoblasts. These results indicate that MeCP2 deficiency leads to altered bone growth. Osteoblast dysfunction was more marked in Mecp2-null male than in HET female mice, suggesting that expression of MeCP2 plays a critical role in bone development.
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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.