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Macrophage migration inhibitory factor (MIF) promotes fibroblast migration in scratch‐wounded monolayers in vitro
Author(s) -
Dewor Manfred,
Steffens Guy,
Krohn Regina,
Weber Christian,
Baron Jens,
Bernhagen Jürgen
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.08.071
Subject(s) - macrophage migration inhibitory factor , fibroblast , wound healing , cell migration , microbiology and biotechnology , cytokine , in vitro , chemistry , cancer research , immunology , receptor , biology , biochemistry
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.