RETRACTED: MicroRNA-326 aggravates acute lung injury in septic shock by mediating the NF-κB signaling pathway

Wu, Chengbin; Huang, Yan; Pei, Zhen-Ye; Xi, Xin; Zhu, Guangfa

doi:10.1016/j.biocel.2018.04.019

Cited by 24 publications

(11 citation statements)

References 42 publications

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“…The formation of NETs has been suggested to be accompanied by the activation of NF‐κB signalling pathway in macrophages, whereas the marginal induction of CXCR1 has been observed in circulating neutrophils recruited by the lung 39,40 . Largely in agreement with our findings, miR‐326 activates the NF‐κB signalling pathway through target inhibition of B cell leukaemia/lymphoma 2–related protein A1, by which inflammatory responses and lung injuries of mice with ALI were aggravated 41 . More importantly, function studies have shown that the inactivation of the NF‐κB signalling pathway can reduce oxidative stress to allow improvement of ALI; CXCR1/2 antagonists can ameliorate LPS‐induced ALI in association with sepsis 42,43 .…”

Section: Discussionsupporting

confidence: 90%

“… 39 , 40 Largely in agreement with our findings, miR‐326 activates the NF‐κB signalling pathway through target inhibition of B cell leukaemia/lymphoma 2–related protein A1, by which inflammatory responses and lung injuries of mice with ALI were aggravated. 41 More importantly, function studies have shown that the inactivation of the NF‐κB signalling pathway can reduce oxidative stress to allow improvement of ALI; CXCR1/2 antagonists can ameliorate LPS‐induced ALI in association with sepsis. 42 , 43 Concordantly, the addition of PDTC, an inhibitor of the NF‐κB signalling pathway, resulted in alleviated lung injuries induced by NET, as observed in mouse models of TRALI in our study.…”

Section: Discussionmentioning

confidence: 99%

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MiR‐144‐induced KLF2 inhibition and NF‐kappaB/CXCR1 activation promote neutrophil extracellular trap–induced transfusion‐related acute lung injury

Liu

et al. 2021

J Cellular Molecular Medi

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

MiR‐144‐induced KLF2 inhibition and NF‐kappaB/CXCR1 activation promote neutrophil extracellular trap–induced transfusion‐related acute lung injury

Liu

et al. 2021

J Cellular Molecular Medi

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“…Recent studies demonstrated that miRNAs function as gene expression switches in key processes of the ALI [33,34]. For example, Wu et al showed that miR-326 targeting the BCL2A1 gene activated the NF-κB signaling pathway, resulting in aggravated inflammatory response and lung injury of septic shock with ALI in mice [35]. Shi et al found that miR-21 inhibitor could aggravate Figure 5.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-27a alleviates LPS-induced acute lung injury in mice via inhibiting inﬂammation and apoptosis through modulating TLR4/MyD88/NF-κB pathway

et al. 2018

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Acute lung injury (ALI) is a critical clinical condition with a high mortality rate, characterized with excessive uncontrolled inflammation and apoptosis. Recently, microRNAs (miRNAs) have been found to play crucial roles in the amelioration of various inflammation-induced diseases, including ALI. However, it remains unknown the biological function and regulatory mechanisms of miRNAs in the regulation of inﬂammation and apoptosis in ALI. The aim of this study is to identify and evaluate the potential role of miRNAs in ALI and reveal the underlying molecular mechanisms of their effects. Here, we analyzed microRNA expression profiles in lung tissues from LPS-challenged mice using miRNA microarray. Because microRNA-27a (miR-27a) was one of the miRNAs being most significantly downregulated, which has an important role in regulation of inflammation, we investigated its function. Overexpression of miR-27a by agomir-27a improved lung injury, as evidenced by the reduced histopathological changes, lung wet/dry (W/D) ratio, lung microvascular permeability and apoptosis in the lung tissues, as well as ameliorative survival of ALI mice. This was accompanied by the alleviating of inflammation, such as the reduced total BALF cell and neutrophil counts, decreased levels of tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-6) interleukin-1β (IL-1β) and myeloperoxidase (MPO) activity in BAL fluid. Toll-like receptor 4 (TLR4), an important regulator of the nuclear factor kappa-B (NF-κB) signaling pathway, was identified as a novel target of miR-27a in RAW264.7 cells. Furthermore, our results showed that LPS stimulation increased the expression of MyD88 and NF-κB p65 (p-p65), but inhibited the expression of inhibitor of nuclear factor-κB-α (IκB-α), suggesting the activation of NF-κB signaling pathway. Further investigations revealed that agomir-miR-27a reversed the promoting effect of LPS on NF-κB signaling pathway. The results here suggested that miR-27a alleviates LPS-induced ALI in mice via reducing inﬂammation and apoptosis through blocking TLR4/MyD88/NF-κB activation.

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“…MiR-155 has been reported to be significantly upregulated in septic lung injury, and its downregulation alleviated inflammation by targeting sirtuin1 (SIRT1) in mouse and cell models [15]. In addition, some other miRNAs have been reported to be promoters or suppressors of ALI, including miR-218 that inhibits RUNX family transcription factor 2 (RUNX2) [16], miR-326 that mediates the NF-κB signaling pathway [17], and others. Here, miR-574-5p expression was decreased in the lung tissues from sepsis model mice, and its overexpression reduced the level of inflammatory factors and the severity of lung injury and in lung endothelial cells by targeting TRAF6.…”

Section: Discussionmentioning

confidence: 99%

MiR-574-5p alleviates sepsis-induced acute lung injury by regulating TRAF6/NF-κB pathway

Xu¹,

Lei²,

Yu³

et al. 2020

Trop. J. Pharm Res

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Purpose: To investigate the protective effect of miR-574-5p pretreatment against acute lung injury (ALI) induced by sepsis.Methods: A male C57BL/6 mouse model of sepsis-induced ALI was established by cecal ligation and puncture (CLP) and treated with miR-574-5p agomir (intravenous injection, 80 mg/kg per day, 3 days). After that, blood and lung samples were obtained for histopathological observation. Myeloperoxidase (MPO) activity, inflammatory cell infiltration, and cytokine expression were analyzed. The target gene of miR-574-5p was predicted using TargetScan prediction, and verified by luciferase assay and western blot.Results: In sepsis-induced ALI mice model, downregulation of miR-574-5p was observed. Pretreatment of miR-574-5p significantly alleviated ALI by suppressing histological damage, and reducing MPO activity and inflammatory cell infiltration, as well as decreasing cytokine expression. The underlying mechanism was that miR-574-5p targeted TNF receptor associated factor 6 (TRAF6) and suppressed the downstream NF-κB pathway. Moreover, TRAF6 overexpression reversed the effects of miR-574-5p on ALI.Conclusion: MiR-574-5p pretreatment suppresses inflammatory responses, thus reducing lung injury induced by sepsis in mice, partly via the regulation of TRAF6 and NF-κB pathway. Therefore, this approach can potentially be used for the clinical management of ALI in humans Keywords: Sepsis, Acute lung injury, MiR-574-5p, TRAF6, NF-κB pathway

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RETRACTED: MicroRNA-326 aggravates acute lung injury in septic shock by mediating the NF-κB signaling pathway

Cited by 24 publications

References 42 publications

MiR‐144‐induced KLF2 inhibition and NF‐kappaB/CXCR1 activation promote neutrophil extracellular trap–induced transfusion‐related acute lung injury

MiR‐144‐induced KLF2 inhibition and NF‐kappaB/CXCR1 activation promote neutrophil extracellular trap–induced transfusion‐related acute lung injury

MicroRNA-27a alleviates LPS-induced acute lung injury in mice via inhibiting inﬂammation and apoptosis through modulating TLR4/MyD88/NF-κB pathway

MiR-574-5p alleviates sepsis-induced acute lung injury by regulating TRAF6/NF-κB pathway

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