MicroRNA-124 alleviates the lung injury in mice with septic shock through inhibiting the activation of the MAPK signaling pathway by downregulating MAPK14

Pan, Weiyun; Wei, Na; Xu, Weiling; Wang, Gang; Gong, Fangchao; Li, Na

doi:10.1016/j.intimp.2019.105835

Cited by 39 publications

(23 citation statements)

References 26 publications

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“…As shown in Figure 1B, it was found that 28 upregulated and 26 down-regulated miRNAs. Among these aberrant miRNAs, miR-124 and miR-16 were decreased, and miR-221 was increased, which are consistent with previous reports [17,[23][24][25], indicating the reliability of our microarray. Let-7e was chose for subsequent investigation due to its important role in regulation of inflammatory response in various diseases [26][27][28].…”

Section: Let-7e Was Upregulated In Lung Tissues and Balf In Ali Micesupporting

confidence: 92%

Down-regulation of miR-let-7e attenuates LPS-induced acute lung injury in mice via inhibiting pulmonary inflammation by targeting SCOS1/NF-κB pathway

Zhang

et al. 2021

Bioscience Reports

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Excessive pulmonary inflammatory response is critical in the development of acute lung injury (ALI). Previously, microRNAs (miRNAs) have been recognized as an important regulator of inflammation in various diseases. However, the effects and mechanisms of miRNAs on inflammatory response in ALI remain unclear. Herein, we tried to screen miRNAs in the processes of ALI and elucidate the potential mechanism. Using a microarray assay, microRNA let-7e (let-7e) was chose as our target for its reported suppressive roles in several inflammatory diseases. Downregulation of let-7e by antagomiR-let-7e injection attenuated LPS-induced acute lung injury. We also found that antagomiR-let-7e could obviously improve the survival rate in ALI mice. Moreover, let-7e inhibition reduced LPS-induced the production of pro-inflammatory cytokines (i.e., TNF-α, IL-1β and IL-6) in bronchoalveolar lavage fluid (BALF). Luciferase reporter assays confirmed that suppressor of cytokine signaling 1 (SOCS1), a powerful attenuator of nuclear factor kappa B (NF-κB) signaling pathway, was directly targeted and suppressed by let-7e in RAW264.7 cells. In addition, it was further observed that SOCS1 was downregulated, and inversely correlated with let-7e expression levels in lung tissues of ALI mice. Finally, downregulation of let-7e suppressed the activation of NF-κB pathway, as evidenced by the reduction of p-IκBα, and nuclear p-p65 expressions in ALI mice. Collectively, our findings indicate that let-7e antagomir protects mice against LPS-induced lung injury via repressing the pulmonary inﬂammation though regulation of SOCS1/NF-κB pathway, and let-7e may act as a potential therapeutic target for ALI.

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Section: Let-7e Was Upregulated In Lung Tissues and Balf In Ali Micesupporting

confidence: 92%

Down-regulation of miR-let-7e attenuates LPS-induced acute lung injury in mice via inhibiting pulmonary inflammation by targeting SCOS1/NF-κB pathway

Zhang

et al. 2021

Bioscience Reports

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“…MiR-124a is highly expressed in the lungs. It exerts a protective effect against acute lung injury by promoting M2 macrophage polarization and suppressing pro-inflammatory responses [58] , [59] , [60] . In a study investigating the microRNA profiling of airway epithelium from lung transplant recipients, miR-124 was significantly downregulated in acute rejection groups than in stable groups.…”

Section: Discussionmentioning

confidence: 99%

Screening and identification of key regulatory connections and immune cell infiltration characteristics for lung transplant rejection using mucosal biopsies

Xiu

Liu

Tang

2020

International Immunopharmacology

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Highlights Identifying hub genes for lung allograft rejection. Constructing a miRNA-TF-mRNA regulatory network in lung allograft rejection. Revealing dysregulation of immune cells during lung allograft rejection. Revealing potential relationships between hub gene expression and immune cell infiltration level. Predicting potential drugs for the treatment of lung allograft rejection.

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“…At present, MAPK1, MAPK3, MAPK6, MAPK14, MAPK12, and MAPK10 are the main researches of MAPK-activated protein kinase 16 . MAP3 K, MAP2 K, and MAPK kinases are located at the highest and lowest positions, respectively, in the canonical three-layer MAPK signaling cascade 17 . There have been a few reports on MAPK signaling pathway in the development of RA 18 , 19 .…”

Section: Introductionmentioning

confidence: 99%

Linc02381 Exacerbates Rheumatoid Arthritis Through Adsorbing miR-590-5p and Activating the Mitogen-Activated Protein Kinase Signaling Pathway in Rheumatoid arthritis-fibroblast-like synoviocytes

Wang

Zhao

2020

Cell Transplant

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Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease. New evidence suggested that linc02381 suppressed colorectal cancer progression by regulating PI3 K signaling pathway, but the role of linc02381 in other diseases, such as RA, remains unclear. This study aimed to reveal the mechanism of linc02381 in RA progression. In vivo and in vitro, we found that linc02381 was upregulated in RA synovial tissues or RA fibroblast-like synoviocytes (RA-FLSs, P < 0.01), which were detected by quantitative real-time polymerase chain reaction. Cell Counting Kit-8, EDU, and Transwell assays revealed that linc02381 overexpression enhanced cell proliferation and invasion, and linc02381 knockdown inhibited cell proliferation and invasion in FLSs. Moreover, the results of bioinformatics analysis, luciferase reporter gene assay, and pull-down assay verified that linc02381 could directly bind with miR-590-5p. MiR-590-5p was downregulated in RA-FLSs, and overexpression of linc02381 suppressed expression of miR-590-5p that post-transcriptionally suppressed the expression of mitogen-activated protein kinase kinase 3 (MAP2K3), and overexpression of miR-590-5p reversed the effect of linc02381 overexpression on MAP2K3 expression. MiR-590-5p inhibitor reversed the inhibition effect of linc02381 knockdown on proliferation and invasion of FLSs, which enhanced expression of MAP2K3, and activation of p38 and AP-1 in the MAPK signaling pathway. In summary, linc02381 was upregulated in RA synovial tissues and RA-FLSs, and it exacerbated RA by adsorbing miR-590-5p to activate the MAPK signaling pathway.

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MicroRNA-124 alleviates the lung injury in mice with septic shock through inhibiting the activation of the MAPK signaling pathway by downregulating MAPK14

Cited by 39 publications

References 26 publications

Down-regulation of miR-let-7e attenuates LPS-induced acute lung injury in mice via inhibiting pulmonary inflammation by targeting SCOS1/NF-κB pathway

Down-regulation of miR-let-7e attenuates LPS-induced acute lung injury in mice via inhibiting pulmonary inflammation by targeting SCOS1/NF-κB pathway

Screening and identification of key regulatory connections and immune cell infiltration characteristics for lung transplant rejection using mucosal biopsies

Linc02381 Exacerbates Rheumatoid Arthritis Through Adsorbing miR-590-5p and Activating the Mitogen-Activated Protein Kinase Signaling Pathway in Rheumatoid arthritis-fibroblast-like synoviocytes

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