Macrophage Migration Inhibitory Factor Up-regulates Matrix Metalloproteinase-9 and -13 in Rat Osteoblasts

Onodera, Shin; Nishihira, Jun; Iwabuchi, Kazuya; Koyama, Yoshikazu; Yoshida, Kazuhiko; Tanaka, Sakae; Minami, Akio

doi:10.1074/jbc.m106020200

Cited by 149 publications

(129 citation statements)

References 62 publications

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“…In fact, MIF is a potent inflammatory mediator, suggesting that it could play a role in the inflammation phase of wound healing, in line with the findings by Ashcroft and colleagues [13]. MIF activates matrix-degrading enzymes such as MMP-1, -9, and -13 [31][32][33][34] and contributes to the mobilization of the extracellular matrix in in vivo wound situations [14], supporting the notion that overexpression of MIF in the inflammation phase encompasses a matrix-turnover function. Of note, recent findings suggest that MIF, contrary to its historic name, promotes the chemotactic recruitment of inflammatory leukocytes into sites of injury such as atherogenic arteries or the inflamed microvasculature [11,35] and can activate the migration of smooth muscle cells [36].…”

Section: Discussionsupporting

confidence: 80%

Macrophage migration inhibitory factor (MIF) promotes fibroblast migration in scratch‐wounded monolayers in vitro

Dewor

Steffens²,

Krohn³

et al. 2007

FEBS Letters

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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.

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Section: Discussionsupporting

confidence: 80%

Macrophage migration inhibitory factor (MIF) promotes fibroblast migration in scratch‐wounded monolayers in vitro

Dewor

Steffens²,

Krohn³

et al. 2007

FEBS Letters

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show abstract

“…This is consistent with the action of exogenous MIF on MAPK/AP-1 activation (3,4,8,9,40,41), and MAPK-dependent control of cell growth and tumorigenesis (7,42,43). In NIH3T3 cells, MIF was required for ERK-induced cell proliferation (3,4,6).…”

Section: Discussionsupporting

confidence: 64%

Regulation of IL-1 and TNF Receptor Expression and Function by Endogenous Macrophage Migration Inhibitory Factor

Toh

Aeberli

Lacey

et al. 2006

The Journal of Immunology

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Macrophage migration inhibitory factor (MIF) has a key role in regulation of innate and adaptive immunity and is implicated in sepsis, tumorigenesis, and autoimmune disease. MIF deficiency or immunoneutralization leads to protection against fatal endotoxic, exotoxic, and infective shock, and anti-inflammatory effects in other experimental models of inflammatory disease. We report a novel regulatory role of MIF in type 1 IL-1R and p55 TNFR expression and function. Compared with wild-type cells, MIF-deficient cells were hyporesponsive to IL-1- and TNF-induced MAPK activity, AP-1 activity, and cellular proliferation, while NF-κB function was preserved. Hyporesponsiveness of MIF-deficient cells was associated with down-regulation of cytokine receptor expression, which was restored by reconstitution of either an upstream kinase of MAPK, MAPK/ERK kinase, or MIF. These data suggest that endogenous MIF is required for cytokine activation of MAPK/AP-1 and cytokine receptor expression. This autocrine regulatory pathway defines an important amplifying role of endogenous MIF in cytokine-mediated immune and inflammatory diseases and provides further molecular evidence for the critical role of MIF in cellular activation.

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“…[5][6][7] Secondly, MIF protein within the synovial fluid of rheumatoid arthritis (RA) patients has been found to be elevated 5-to 10-fold higher than that seen in osteoarthritis patients and normal volunteers. 12 Thirdly, MIF is known to induce macrophage tumour necrosis factor a (TNFa) release and nitric oxide production, as well as being involved in T-cell activation, all of which play a role in RA pathogenesis. Fourthly, immunostaining of MIF within the RA synovium is strongly correlated with disease activity, as measured by CRP.…”

Section: Discussionmentioning

confidence: 99%

Macrophage migration inhibitory factor (MIF) gene polymorphism is associated with susceptibility to but not severity of inflammatory polyarthritis

et al. 2003

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Macrophage Migration Inhibitory Factor Up-regulates Matrix Metalloproteinase-9 and -13 in Rat Osteoblasts

Cited by 149 publications

References 62 publications

Macrophage migration inhibitory factor (MIF) promotes fibroblast migration in scratch‐wounded monolayers in vitro

Macrophage migration inhibitory factor (MIF) promotes fibroblast migration in scratch‐wounded monolayers in vitro

Regulation of IL-1 and TNF Receptor Expression and Function by Endogenous Macrophage Migration Inhibitory Factor

Macrophage migration inhibitory factor (MIF) gene polymorphism is associated with susceptibility to but not severity of inflammatory polyarthritis

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