Protection from Gao-Binge induced liver injury in Mif–/– Mice is associated with decreased ER stress

Poulsen, Kyle L.; McMullen, Megan R.; Sheehan, Michael J.; Leng, Liang; Bucala, Richard; Nagy, Laura E.

doi:10.1016/s0168-8278(18)30313-1

Cited by 3 publications

(1 citation statement)

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“…Although the direct correlation between DENV-induced ER stress and MIF secretion has not been elucidated, both MIF and ER stress can induce autophagy through ERK1/2 phosphorylation [58,59] and ROS generation [60]. Interestingly, MIF is able to induce ER stress in a liver injury model [61]. Therefore, it is possible that MIF signal transduction may trigger ER stress and ERK activation upon DENV infection, leading to autophagy induction and viral replication, or vice versa.…”

Section: Mif Enhances Denv Replication In Host Cellsmentioning

confidence: 99%

Roles of Macrophage Migration Inhibitory Factor in Dengue Pathogenesis: From Pathogenic Factor to Therapeutic Target

2020

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Dengue virus (DENV) infection is the most prevalent mosquito-borne viral infection and can lead to severe dengue hemorrhagic fever (DHF) and even life-threatening dengue shock syndrome (DSS). Although the cytokine storm has been revealed as a critical factor in dengue disease, the limited understanding of dengue immunopathogenesis hinders the development of effective treatments. Macrophage migration inhibitory factor (MIF) is a pleiotropic proinflammatory cytokine that mediates diverse immune responses, and the serum level of MIF positively correlates with disease severity in patients with dengue. MIF is involved in DENV replication and many pathological changes, such as vascular leakage, during DENV infection. In this paper, the pathogenic roles of MIF and the regulation of MIF secretion during DENV infection are reviewed. Furthermore, whether MIF is a potential therapeutic target against DENV infection is also discussed.

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Section: Mif Enhances Denv Replication In Host Cellsmentioning

confidence: 99%

Roles of Macrophage Migration Inhibitory Factor in Dengue Pathogenesis: From Pathogenic Factor to Therapeutic Target

2020

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The Role of MIF in Hepatic Function, Oxidative Stress, and Inflammation in Thioacetamide-induced Liver Injury in Mice: Protective Effects of Betaine

Vukićević

Rovčanin

Gopčević

et al. 2021

CMC

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Background: Macrophage migration inhibitory factor (MIF) is a multipotent cytokine that contributes to the inflammatory response to chemical liver injury. This cytokine exhibits pro- and anti-inflammatory effects depending on etiology and stage of liver disease. Objective: Our study aimed to investigate the role of MIF in oxidative stress and the inflammation in the liver, and modulatory effects of betaine on MIF in thioacetamide (TAA)-induced chronic hepatic damage in mice. Methods: The experiment was performed on wild type and knockout MIF-/- C57BL/6 mice. They were divided into groups: Control; Bet-group, received betaine (2% wt/v dissolved in drinking water); MIF-/- mice group; MIF-/-+Bet; TAA-group, received of TAA (200 mg/kg b.w.), intraperitoneally, 3x/week/8 weeks); TAA+Bet; MIF-/-+TAA, and MIF-/-+TAA+Bet. In TAA- and Bet-treated groups, animals received in the same previous doses. After eight weeks of treatment, blood samples were collected for biochemical analysis and liver specimens were prepared for assessment the parameters of oxidative stress and inflammation. Results: In MIF-/-mice, TAA reduced transaminases, -glutamyltranspeptidase, bilirubin, malondaldehyde (MDA), oxidative protein products (AOPP), total oxidant status (TOS), C-reactive protein (CRP), IL-6, IFN- , and increased of thiols and total antioxidant status (TAS). Betain attenuates mechanism of MIF-mediated effects in TAA-induced liver injury, reducing transaminases, -glutamyltranspeptidase, bilirubin, MDA, AOPP, TOS, CRP, IL-6, IFN-g and increasing thiols. Conclusion: MIF is mediator in hepatotoxic, pro-oxidative and proinfammatory effects of TAA-induced liver injury. MIFtargeted therapy could potentially mitigate the oxidative stress and inflammation in the liver, but the exact mechanism of its action requires further investigation. Betaine increases antioxidative defense and attenuates hepatotoxic effects of MIF, suggesting that betaine can be used for the prevention and treatment of liver damage.

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Betaine Modulating MIF-Mediated Oxidative Stress, Inflammation and Fibrogenesis in Thioacetamide-Induced Nephrotoxicity

Jorgačević

Stankovic

Filipović³

et al. 2022

CMC

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Background: Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine with chemokine properties released by various immune and nonimmune cells. It contributes to the pathogenesis of many inflammatory, autoimmune diseases and malignant tumors. Objective: Our study aimed to investigate the role of betaine in the modulation of MIF-mediated oxidative stress, inflammation, and fibrogenesis during toxic kidney damage induced by thioacetamide (TAA). Methods: The experiment is performed on wild-type and knockout MIF-/- C57BL/6 mice. They are randomly divided into groups: Control; Bet-group, received betaine (2% wt/v dissolved in drinking water); MIF-/- mice group; MIF-/-+Bet; TAA-group, treated with TAA (200 mg/kg b.w.), intraperitoneally, 3x/week/8 weeks); TAA+Bet; MIF-/-+TAA, and MIF-/-+TAA+Bet group. After eight weeks of treatment, animals are sacrificed and kidney samples are taken to determine oxidative stress parameters, proinflammatory cytokines, profibrogenic factors, and histopathology of renal tissue Results: In MIF-/-mice, TAA decreases malondialdehyde (MDA) concentration, IL-6, tumor necrosis factor-alpha (TNF-, transforming growth factor-beta 1 (TGF-1) and plateled-derived growth factor-BB (PDGF-BB) and increases superoxide dismutases (SOD) and catalase (CAT) activities, as well as glutathione (GSH) content in kidneys, compared to TAA group. Betaine alleviates the mechanism of MIF-mediated effects in TAA-induced nephrotoxicity, reducing MDA, IL-6, TNF-, TGF-1, and PDGF-BB, and increasing SOD and CAT activity, as well as GSH levels. Conclusion: MIF mediates TAA-induced nephrotoxicity by increasing oxidative stress, inflammation, and profibrogenic mediators. MIF-targeted therapy could potentially alleviate oxidative stress and inflammation in the kidney, as well as pathohistological changes in renal tissue, but the exact mechanism of its action is not completely clear. Betaine alleviates MIF nephrotoxic effects by increasing the antioxidative capacity of kidney cells, and decreasing lipid peroxidation and cytokine production in the renal tissue. It suggests that betaine can be used for the prevention of kidney damage.

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Protection from Gao-Binge induced liver injury in Mif–/– Mice is associated with decreased ER stress

Cited by 3 publications

References 0 publications

Roles of Macrophage Migration Inhibitory Factor in Dengue Pathogenesis: From Pathogenic Factor to Therapeutic Target

Roles of Macrophage Migration Inhibitory Factor in Dengue Pathogenesis: From Pathogenic Factor to Therapeutic Target

The Role of MIF in Hepatic Function, Oxidative Stress, and Inflammation in Thioacetamide-induced Liver Injury in Mice: Protective Effects of Betaine

Betaine Modulating MIF-Mediated Oxidative Stress, Inflammation and Fibrogenesis in Thioacetamide-Induced Nephrotoxicity

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