Macrophage migration inhibitory factor promotes renal injury induced by ischemic reperfusion

Autor: Jun Lv, Zhi H. Zheng, Zi J Zhou, Hui Yang, Qiu Y. Huang, Xiao H. Wang, Andreas Meinhardt, Jörg Klug, Hui-Yao Lan, Patrick Ming-Kuen Tang, Gunter Fingerle-Rowson, Ying Tang, Jin H Li, Xiao R. Huang, Zhi J. He, An P. Xu
Rok vydání: 2019
Předmět:
Male
0301 basic medicine
CD74
medicine.medical_treatment
Kidney
urologic and male genital diseases
Mice
chemistry.chemical_compound
0302 clinical medicine
Chemokine CCL2
Mice
Knockout
NF-kappa B
Acute kidney injury
Acute Kidney Injury
Middle Aged
female genital diseases and pregnancy complications
Intramolecular Oxidoreductases
Cytokine
medicine.anatomical_structure
Creatinine
Reperfusion Injury
030220 oncology & carcinogenesis
Disease Progression
Molecular Medicine
Original Article
Female
renal inflammation
Adult
medicine.medical_specialty
Urinary system
chemical and pharmacologic phenomena
macrophage migration inhibitory factor (MIF)
03 medical and health sciences
Internal medicine
otorhinolaryngologic diseases
medicine
Animals
Humans
Macrophage Migration-Inhibitory Factors
CXCL15
Aged
urogenital system
business.industry
Histocompatibility Antigens Class II
Original Articles
Cell Biology
medicine.disease
cytokines
Antigens
Differentiation
B-Lymphocyte
Mice
Inbred C57BL
Toll-Like Receptor 4
Disease Models
Animal
030104 developmental biology
Endocrinology
chemistry
Macrophage migration inhibitory factor
business
Zdroj: Journal of Cellular and Molecular Medicine
ISSN: 1582-4934
1582-1838
Popis: 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.
Databáze: OpenAIRE
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