ArticlePloS one2015
The Tissue Fibrinolytic System Contributes to the Induction of Macrophage Function and CCL3 during Bone Repair in Mice.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Hdac3 deficiency limits periosteal reaction associated with Western diet feeding in female mice.Journal of cellular and molecular medicine · 2024Article
- The emerging role of tranexamic acid and its principal target, plasminogen, in skeletal health.Acta pharmaceutica Sinica. B · 2024Review
- Systemic Inflammatory Regulators Associated with Osteoporosis: A Bidirectional Mendelian Randomization Study.Calcified tissue international · 2024Article
- Review
- Role of Macrophages and Plasminogen Activator Inhibitor-1 in Delayed Bone Repair Induced by Glucocorticoids in Mice.International journal of molecular sciences · 2022Article
- Article
- Plasminogen activation in the musculoskeletal acute phase response: Injury, repair, and disease.Research and practice in thrombosis and haemostasis · 2020Review
- Roles of fibrinolytic factors in the alterations in bone marrow hematopoietic stem/progenitor cells during bone repair.Inflammation and regeneration · 2020Review
- Article
- Chemokines in Physiological and Pathological Bone Remodeling.Frontiers in immunology · 2019Review
- Shear and Dynamic Compression Modulates the Inflammatory Phenotype of Human MonocytesFrontiers in immunology · 2019Article
- Correlation of Serum CCL3/MIP-1α Levels with Disease Severity in Postmenopausal Osteoporotic FemalesBalkan medical journal · 2018Article
- Roles of plasminogen in the alterations in bone marrow hematopoietic stem cells during bone repair.Bone reports · 2018Article
- Osteomacs and Bone Regeneration.Current osteoporosis reports · 2017Review
- Macrophage Transplantation Fails to Improve Repair of Critical-Sized Calvarial Defects.The Journal of craniofacial surgeryArticle
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages play crucial roles in repair process of various tissues. However, the details in the role of macrophages during bone repair still remains unknown. Herein, we examined the contribution of the tissue fibrinolytic system to the macrophage functions in bone repair after femoral bone defect by using male mice deficient in plasminogen (Plg-/-), urokinase-type plasminogen activator (uPA-/-) or tissue-type plasminogen activator (tPA-/-) genes and their wild-type littermates. Bone repair of the femur was delayed in uPA-/- mice until day 6, compared with wild-type (uPA+/+) mice. Number of Osterix-positive cells and vessel formation were decreased in uPA-/- mice at the bone injury site on day 4, compared with those in uPA+/+ mice. Number of macrophages and their phagocytosis at the bone injury site were reduced in uPA-/- and Plg-/-, but not in tPA-/- mice on day 4. Although uPA or plasminogen deficiency did not affect the levels of cytokines, including TNF-α, IL-1β, IL-6, IL-4 and IFN-γ mRNA in the damaged femur, the elevation in CCL3 mRNA levels was suppressed in uPA-/- and Plg-/-, but not in tPA-/- mice. Neutralization of CCL3 antagonized macrophage recruitment to the site of bone injury and delayed bone repair in uPA+/+, but not in uPA-/- mice. Our results provide novel evidence that the tissue fibrinolytic system contributes to the induction of macrophage recruitment and CCL3 at the bone injury site, thereby, leading to the enhancement of the repair process.
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