ArticleOsteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA2011
Impaired fracture healing in macrophage migration inhibitory factor-deficient mice.
Article in Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Protein compound macrophage migration inhibitory factor for diagnosing postmenopausal osteoporosis.Frontiers in chemistry · 2026Article
- Addressing the challenges of infectious bone defects: a review of recent advances in bifunctional biomaterials.Journal of nanobiotechnology · 2025Review
- Callus organoids reveal distinct cartilage to bone transition mechanisms across donors and a role for biological sex.Bone research · 2025Article
- The role of macrophages in fracture healing: a narrative review of the recent updates and therapeutic perspectives.Stem cell investigation · 2023Review
- Macrophage-Mediated Bone Formation in Scaffolds Modified With MSC-Derived Extracellular Matrix Is Dependent on the Migration Inhibitory Factor Signaling Pathway.Frontiers in cell and developmental biology · 2021Article
- Time Course of Immune Response and Immunomodulation During Normal and Delayed Healing of Musculoskeletal Wounds.Frontiers in immunology · 2020Review
- Hypoxia and mesenchymal stromal cells as key drivers of initial fracture healing in an equine in vitro fracture hematoma model.PloS one · 2019Article
- Cellular biology of fracture healing.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2019Review
- A Translational Model of Incomplete Catch-Up Growth: Early-Life Hypoxia and the Effect of Physical Activity.Clinical and translational science · 2018Article
- The Association of Higher Plasma Macrophage Migration Inhibitory Factor Levels with Lower Bone Mineral Density and Higher Bone Turnover Rate in Postmenopausal Women.Endocrinology and metabolism (Seoul, Korea) · 2016Article
- Macrophage migration inhibitory factor is essential for osteoclastogenic mechanisms in vitro and in vivo mouse model of arthritis.Cytokine · 2015Article
- Clinical therapeutic effects of anterior decompression on spinal osteoporotic fracture and inflammatory cytokines.Pakistan journal of medical sciences · 2014Article
- Hyperbaric hyperoxia accelerates fracture healing in mice.PloS one · 2013Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledThis study investigated the role of macrophage migration inhibitory factor (MIF) in fracture repair using MIF gene-deficient mice (MIF KO). Fracture healing was delayed in MIF KO, and this was mainly due to the delay in the mineralization of osteoid within the fracture callus.
introductionWe previously reported that the expression of macrophage migration inhibitory factor (MIF) was up-regulated during the fracture healing process in rats. However, its role in the pathophysiology of this process remained unclear. The aim of the present study was to clarify the role of MIF in the fracture healing process using MIF gene-deficient mice (MIF KO).
methodsBone repair in wild-type mice (WT) and MIF KO (n = 70, respectively) was investigated using a tibia fracture model. Radiographic, biomechanical, histological, bone histomorphometric, and molecular analyses were performed.
resultsPost-fracture biomechanical testing showed that maximum load and stiffness were significantly lower in MIF KO than in WT on day 42. However, similar levels were observed between the two groups on day 84. Bone histomorphometric analysis revealed significantly higher osteoid volume, a lower mineral apposition rate, and smaller numbers of osteoclasts in the MIF KO callus compared to the WT callus. The messenger ribonucleic acid expressions of matrix metalloproteinase (MMP)-2, membranous type 1-MMP, cathepsin K, and tissue nonspecific alkaline phosphatase were found to be significantly suppressed in the MIF KO callus.
conclusionThe results of the present study suggest that delayed fracture healing in MIF KO was mainly attributable to a delay in osteoid mineralization.
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