Macrophage migration inhibitory factor (MIF) promotes fibroblast migration in scratch-wounded monolayers in vitro
Autor: | Christian Weber, Guy C. M. Steffens, Regina M. Krohn, Jens M. Baron, Manfred Dewor, Jürgen Bernhagen |
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Rok vydání: | 2007 |
Předmět: |
Leukocyte migration
Time Factors animal diseases medicine.medical_treatment Biophysics Wound healing Down-Regulation chemical and pharmacologic phenomena Inflammation Biology Biochemistry CXCR4 Fibroblast migration Mice Cell Movement Structural Biology otorhinolaryngologic diseases Genetics medicine Animals Humans Calcium Signaling Fibroblast Macrophage Migration-Inhibitory Factors Molecular Biology Migration Cells Cultured Cell Proliferation MIF Cell Biology Fibroblasts respiratory system biological factors Cell biology medicine.anatomical_structure Cytokine Immunology Wounds and Injuries Macrophage migration inhibitory factor medicine.symptom |
Zdroj: | FEBS Letters. 581:4734-4742 |
ISSN: | 0014-5793 |
DOI: | 10.1016/j.febslet.2007.08.071 |
Popis: | MIF was recently redefined as an inflammatory cytokine, which functions as a critical mediator of diseases such as septic shock, rheumatoid arthritis, atherosclerosis, and cancer. MIF also regulates wound healing processes. Given that fibroblast migration is a central event in wound healing and that MIF was recently demonstrated to promote leukocyte migration through an interaction with G-protein-coupled receptors, we investigated the effect of MIF on fibroblast migration in wounded monolayers in vitro. Transient but not permanent exposure of primary mouse or human fibroblasts with MIF significantly promoted wound closure, a response that encompassed both a proliferative and a pro-migratory component. Importantly, MIF-induced fibroblast activation was accompanied by an induction of calcium signalling, whereas chronic exposure with MIF down-regulated the calcium transient, suggesting receptor desensitization as the underlying mechanism. |
Databáze: | OpenAIRE |
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