ArticleHaematologica2016
Wnt5a is a key target for the pro-osteogenic effects of iron chelation on osteoblast progenitors.
Article in Haematologica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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31 citing papers in PubMed, 68 citations in OpenAlex.
- 4-Octyl Itaconate Attenuates Postmenopausal Osteoporosis by Inhibiting Ferroptosis and Enhancing Osteogenesis via the Nrf2 Pathway.Inflammation · 2025Article
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- Bone phenotype in male and female mice after knockdown of transferrin receptor 1 in osterix-expressing cells.JBMR plus · 2025Article
- Iron metabolism in rheumatic diseases.Journal of translational autoimmunity · 2025Review
- The Roles of DMT1 in Inflammatory and Degenerative Diseases.Molecular neurobiology · 2025Review
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- Three signalling pathways for iron overload in osteoporosis: a narrative review.Journal of orthopaedic surgery and research · 2025Review
- Iron and Bone Pathophysiology.Advances in experimental medicine and biology · 2025Review
- The role of ferroptosis in osteoporosis: from pathogenic mechanisms to natural product-driven therapeutic innovations.Frontiers in medicine · 2025Review
- Article
- The influence of iron on bone metabolism disorders.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2024Review
- Wnt5a deficiency in osteocalcin-expressing cells could not alleviate the osteoarthritic phenotype in a mouse model of post-traumatic osteoarthritis.Iranian journal of basic medical sciences · 2024Article
- Role of Iron Accumulation in Osteoporosis and the Underlying Mechanisms.Current medical science · 2023Article
- The Role of Trace Elements and Minerals in Osteoporosis: A Review of Epidemiological and Laboratory Findings.Biomolecules · 2023Review
- Fighting age-related orthopedic diseases: focusing on ferroptosis.Bone research · 2023Review
- Dietary intervention reprograms bone marrow cellular signaling in obese mice.Frontiers in endocrinology · 2023Article
- Emerging Roles of the Iron Chelators in Inflammation.International journal of molecular sciences · 2022Review
- Canonical Wnt Signaling in the Pathology of Iron Overload-Induced Oxidative Stress and Age-Related Diseases.Oxidative medicine and cellular longevity · 2022Review
- Article
- Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iron overload due to hemochromatosis or chronic blood transfusions has been associated with the development of osteoporosis. However, the impact of changes in iron homeostasis on osteoblast functions and the underlying mechanisms are poorly defined. Since Wnt signaling is a critical regulator of bone remodeling, we aimed to analyze the effects of iron overload and iron deficiency on osteoblast function, and further define the role of Wnt signaling in these processes. Therefore, bone marrow stromal cells were isolated from wild-type mice and differentiated towards osteoblasts. Exposure of the cells to iron dose-dependently attenuated osteoblast differentiation in terms of mineralization and osteogenic gene expression, whereas iron chelation with deferoxamine promoted osteogenic differentiation in a time- and dose-dependent manner up to 3-fold. Similar results were obtained for human bone marrow stromal cells. To elucidate whether the pro-osteogenic effect of deferoxamine is mediated via Wnt signaling, we performed a Wnt profiler array of deferoxamine-treated osteoblasts. Wnt5a was amongst the most highly induced genes. Further analysis revealed a time- and dose-dependent induction of Wnt5a being up-regulated 2-fold after 48 h at 50 μM deferoxamine. Pathway analysis using specific inhibitors revealed that deferoxamine utilized the phosphatidylinositol-3-kinase and nuclear factor of activated T cell pathways to induce Wnt5a expression. Finally, we confirmed the requirement of Wnt5a in the deferoxamine-mediated osteoblast-promoting effects by analyzing the matrix mineralization of Wnt5a-deficient cells. The promoting effect of deferoxamine on matrix mineralization in wild-type cells was completely abolished in Wnt5a
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