Macrophage migration inhibitory factor promotes renal injury induced by ischemic reperfusion.
Acute Kidney Injury
/ blood
Adult
Aged
Animals
Antigens, Differentiation, B-Lymphocyte
/ metabolism
Chemokine CCL2
/ metabolism
Creatinine
/ blood
Cytokines
/ blood
Disease Models, Animal
Disease Progression
Female
Histocompatibility Antigens Class II
/ metabolism
Humans
Intramolecular Oxidoreductases
/ blood
Kidney
/ immunology
Macrophage Migration-Inhibitory Factors
/ blood
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Middle Aged
NF-kappa B
/ metabolism
Reperfusion Injury
/ blood
Toll-Like Receptor 4
/ metabolism
acute kidney injury
cytokines
macrophage migration inhibitory factor (MIF)
renal inflammation
Journal
Journal of cellular and molecular medicine
ISSN: 1582-4934
Titre abrégé: J Cell Mol Med
Pays: England
ID NLM: 101083777
Informations de publication
Date de publication:
06 2019
06 2019
Historique:
received:
16
08
2018
revised:
27
11
2018
accepted:
16
12
2018
pubmed:
11
4
2019
medline:
31
7
2020
entrez:
11
4
2019
Statut:
ppublish
Résumé
Macrophage migration inhibitory factor (MIF) is pleiotropic cytokine that has multiple effects in many inflammatory and immune diseases. This study reveals a potential role of MIF in acute kidney injury (AKI) in patients and in kidney ischemic reperfusion injury (IRI) mouse model in MIF wild-type (WT) and MIF knockout (KO) mice. Clinically, plasma and urinary MIF levels were largely elevated at the onset of AKI, declined to normal levels when AKI was resolved and correlated tightly with serum creatinine independent of disease causes. Experimentally, MIF levels in plasma and urine were rapidly elevated after IRI-AKI and associated with the elevation of serum creatinine and the severity of tubular necrosis, which were suppressed in MIF KO mice. It was possible that MIF may mediate AKI via CD74/TLR4-NF-κB signalling as mice lacking MIF were protected from AKI by largely suppressing CD74/TLR-4-NF-κB associated renal inflammation, including the expression of MCP-1, TNF-α, IL-1β, IL-6, iNOS, CXCL15(IL-8 in human) and infiltration of macrophages, neutrophil, and T cells. In conclusion, our study suggests that MIF may be pathogenic in AKI and levels of plasma and urinary MIF may correlate with the progression and regression of AKI.
Identifiants
pubmed: 30968541
doi: 10.1111/jcmm.14234
pmc: PMC6533527
doi:
Substances chimiques
Antigens, Differentiation, B-Lymphocyte
0
Ccl2 protein, mouse
0
Chemokine CCL2
0
Cytokines
0
Histocompatibility Antigens Class II
0
Macrophage Migration-Inhibitory Factors
0
NF-kappa B
0
Tlr4 protein, mouse
0
Toll-Like Receptor 4
0
invariant chain
0
Creatinine
AYI8EX34EU
Intramolecular Oxidoreductases
EC 5.3.-
MIF protein, human
EC 5.3.2.1
Mif protein, mouse
EC 5.3.2.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3867-3877Informations de copyright
© 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
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