MCP-induced protein 1 attenuates sepsis-induced acute lung injury by modulating macrophage polarization via the JNK/c-Myc pathway

Zhang, Jiatong; Huang, Tianfeng; Jiang, Lulu; Gao, Ju; Yu, Dapeng; Ge, Yali; Lin, Shunyan

doi:10.1016/j.intimp.2019.105741

Cited by 43 publications

(42 citation statements)

References 37 publications

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“…To determine the role of MCPIP-1 in regulating neutrophil functions, we cultured neutrophils from patients with active IBD and healthy controls in vitro and induced them to overexpress MCPIP-1 by MG-132, a proteasome inhibitor that induces overexpression of MCPIP-1 in several cell types by reducing the degradation of MCPIP-1 [ 26 , 33 ]. We confirmed that MG-132 markedly promoted neutrophils to express MCPIP-1 (Figures 2(a) and 2(b) ).…”

Section: Resultsmentioning

confidence: 99%

“…It may be ascribed to accumulation of MCPIP-1 in limiting the synthesis of itself [ 23 ]. As a proteasome inhibitor, MG-132 is observed to enhance MCPIP-1 expression in several types of immune cells by inhibiting the degradation of MCPIP-1 [ 26 , 33 ], and it also inhibits the activity of NF- κ B in vivo [ 47 ]. In addition, a previous study has also reported that MG-132 could alleviate the experimental colitis in mice via mediating the immunoinhibitory effects on CD4 + T cells [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

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Monocyte Chemotactic Protein 1-Induced Protein 1 Is Highly Expressed in Inflammatory Bowel Disease and Negatively Regulates Neutrophil Activities

Lin

et al. 2020

Mediators of Inflammation

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Monocyte chemotactic protein 1-induced protein 1 (MCPIP-1) is highly expressed in activated immune cells and plays an important role in negatively regulating immune responses. However, its role in regulating neutrophil functions in the pathogenesis of inflammatory bowel disease (IBD) is still unclear. Here, we found that MCPIP-1 was markedly increased at both the transcriptional and translational levels in inflamed mucosa of IBD patients compared with healthy controls, which was mainly expressed in neutrophils. Interestingly, MG-132, a proteasome inhibitor reducing the degradation of MCPIP-1, further facilitated neutrophils to express MCPIP-1 in vitro. Importantly, MCPIP-1 markedly downregulated the production of ROS, MPO, and proinflammatory cytokines (e.g., interleukin-1β, interleukin-6, tumor necrosis factor-α, interleukin-8, and interferon-γ) and suppressed the migration of IBD neutrophils. Consistently, the same functional changes were observed in neutrophils from mice with myeloid-targeted overexpression of MCPIP-1 as MG-132 did. Altogether, these findings suggest that MCPIP-1 plays a negative role in regulating neutrophil activities through suppressing the production of ROS, MPO, and proinflammatory cytokines and inhibiting the migration. MG-132 may partially modulate the function of neutrophils via the induction of MCPIP-1. Therefore, targeting MCPIP-1 or exogenous supplementation of MG-132 may provide a therapeutic approach in the treatment of IBD.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Monocyte Chemotactic Protein 1-Induced Protein 1 Is Highly Expressed in Inflammatory Bowel Disease and Negatively Regulates Neutrophil Activities

Lin

et al. 2020

Mediators of Inflammation

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“…Studies have also shown that the inhibition of c-Myc could give rise to a suppression in proinflammatory signaling. Zhang et al 47 reported that MCP-induced protein 1 could relieve LPS-induced ALI and inflammation by modulating c-Myc-mediated macrophage polarization. Our study demonstrated that c-Myc was upregulated in macrophages during ALI, and c-Myc served as a transcription factor of STING and was responsible for transcriptional activation by directly binding to promoter of STING and enhancing promoter activity, indicating that c-Myc was also involved in the transcription of genes associated with innate immunity and inflammation.…”

Section: Discussionmentioning

confidence: 99%

Cytosolic DNA‐STING‐NLRP3 axis is involved in murine acute lung injury induced by lipopolysaccharide

Wang

Jiang

et al. 2020

Clinical & Translational Med

162

125

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“…Macrophage produces nutrition factors and nerve toxicity factors, and shows the dual role of proinflammatory and anti-inflammatory, characterized by M1 and M2 polarization (32)(33)(34). M1 macrophage secretes high levels of oxide metabolites and proinflammatory factor, such as IL-6 and TNF-α.…”

Section: Discussionmentioning

confidence: 99%

Propofol inhibits inflammatory response by regulating the miR-494/ Nrdp1 pathway in ICH mice model

Shi

Xiong

Huang

et al. 2020

Preprint

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Background: Propofol is an anesthetic agent with neuro-protective effect in neuronal injury. However, the mechanism of propofol in M1 macrophage polarization following ICH has not been well studied. Ubiquitination mediated M1/M2 macrophage polarization plays important roles in pathogenesis of immune disease. The experiment analyzed anti-inflammatory effects of propofol in macrophages following ICH. Methods: In the experiment, macrophages were administrated with erythrocyte lysates, and then miR-494, Nrdp1 and M1 related markers were analyzed. In addition, brain inflammatory response, brain edema, and neurological functions of ICH mice were also assessed. Results: We found that propofol decreased miR-494 levels while increased Nrdp1 levels in macrophages after ICH. We also demonstrated that miR-494 inhibited Nrdp1 expression by directly binding its 3′-untranslated region. MiR-494 attenuated Nrdp1 levels and downstream proinflammatory factors production. Upregulation of Nrdp1 in macrophages significantly decreased M1 macrophage polarization. Conclusion: Taken together, these results suggest that propofol can attenuate the neuroinflammatory response of macrophages after ICH through regulation of the miR-494/Nrdp1 pathway.

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MCP-induced protein 1 attenuates sepsis-induced acute lung injury by modulating macrophage polarization via the JNK/c-Myc pathway

Cited by 43 publications

References 37 publications

Monocyte Chemotactic Protein 1-Induced Protein 1 Is Highly Expressed in Inflammatory Bowel Disease and Negatively Regulates Neutrophil Activities

Monocyte Chemotactic Protein 1-Induced Protein 1 Is Highly Expressed in Inflammatory Bowel Disease and Negatively Regulates Neutrophil Activities

Cytosolic DNA‐STING‐NLRP3 axis is involved in murine acute lung injury induced by lipopolysaccharide

Propofol inhibits inflammatory response by regulating the miR-494/ Nrdp1 pathway in ICH mice model

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