ArticleBone2016
Deletion of the membrane complement inhibitor CD59a drives age and gender-dependent alterations to bone phenotype in mice.
Article in Bone, 2016. 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, 21 citations in OpenAlex.
- Genetic Determinants of Treatment-Related Bone Toxicity in Pediatric Acute Lymphoblastic Leukemia.Clinical pharmacology and therapeutics · 2026Article
- Role of Complement Component 9 in Bone Health: Causal Evidence in Humans and Mechanistic Studies in Mice.Calcified tissue international · 2026Article
- Collectin-11 regulates osteoclastogenesis and bone maintenance via a complement-dependent mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- C3a-C3aR signaling is a novel modulator of skeletal homeostasis.Bone reports · 2023Article
- New insight of complement system in the process of vascular calcification.Journal of cellular and molecular medicine · 2023Review
- Multiple CD59 Polymorphisms in Chinese Patients withJournal of immunology research · 2023Article
- The Implications of Bone Marrow Adipose Tissue on Inflammaging.Frontiers in endocrinology · 2022Review
- Inhibition of miR-29 Activity in the Myeloid Lineage Increases Response to Calcitonin and Trabecular Bone Volume in Mice.Endocrinology · 2021Article
- Article
- Terminal complement complex formation is associated with intervertebral disc degeneration.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 · 2021Article
- Sexual Dimorphism in Osteoclasts.Cells · 2020Review
- Rac1 Inhibition Via Srgap2 Restrains Inflammatory Osteoclastogenesis and Limits the Clastokine, SLIT3.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- Ageing characteristics of bone indicated by transcriptomic and exosomal proteomic analysis of cortical bone cells.Journal of orthopaedic surgery and research · 2019Article
- Inhibition of CCL3 abrogated precursor cell fusion and bone erosions in human osteoclast cultures and murine collagen-induced arthritis.Rheumatology (Oxford, England) · 2018Article
- Osteoarthritis and the Complement Cascade.Clinical medicine insights. Arthritis and musculoskeletal disorders · 2018Review
- The complement system as a potential therapeutic target in rheumatic disease.Nature reviews. Rheumatology · 2017Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Degenerative joint diseases such as osteoarthritis are characterised by aberrant region-specific bone formation and abnormal bone mineral content. A recent study suggested a role for the complement membrane attack complex in experimental models of osteoarthritis. Since CD59a is the principal regulator of the membrane attack complex in mice, we evaluated the impact of CD59a gene deletion upon maintenance of bone architecture. In vivo bone morphology analysis revealed that male CD59a-deficient mice have increased femur length and cortical bone volume, albeit with reduced bone mineral density. However, this phenomenon was not observed in female mice. Histomorphometric analysis of the trabecular bone showed increased rates of bone homeostasis, with both increased bone resorption and mineral apposition rate in CD59a-deficient male mice. When bone cells were studied in isolation, in vitro osteoclastogenesis was significantly increased in male CD59a-deficient mice, although osteoblast formation was not altered. Our data reveal, for the first time, that CD59a is a regulator of bone growth and homeostasis. CD59a ablation in male mice results in longer and wider bones, but with less density, which is likely a major contributing factor for their susceptibility to osteoarthritis. These findings increase our understanding of the role of complement regulation in degenerative arthritis.
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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.