MicroRNAs: Novel regulatory molecules in acute lung injury/acute respiratory distress syndrome

Cao, Yongmei; Lyu, Yuanyuan; Tang, Jia-Hua; Li, Yingchuan

doi:10.3892/br.2016.620

Cited by 42 publications

(44 citation statements)

References 41 publications

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“…According to existing research, an obvious reduction of miR‐27b has been observed in several NSCLC cell lines, and the forced overexpression of miR‐27 could suppress cell proliferation and invasion of NSCLC (J. Jiang et al, ). The experimental data of other study is in consistency with our findings, thereby supporting that miR‐27b was upregulated in ALI and deregulated miR‐27b is beneficial to ALI (Cao, Lyu, Tang, & Li, ).…”

Section: Discussionsupporting

confidence: 91%

Downregulated microRNA‐27b attenuates lipopolysaccharide‐induced acute lung injury via activation of NF‐E2‐related factor 2 and inhibition of nuclear factor κB signaling pathway

Huang

Zhu

et al. 2018

Journal Cellular Physiology

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Acute lung injury (ALI) is a life-threatening, diffuse heterogeneous lung injury characterized by acute onset, pulmonary edema, and respiratory failure. Lipopolysaccharide (LPS) is a leading cause for ALI and when administered to a mouse it induces a lung phenotype exhibiting some of the clinical characteristics of human ALI.This study focused on investigating whether microRNA-27b (miR-27b) affects ALI in a mouse model established by LPS-induction and to further explore the underlying mechanism. After model establishment, the mice were treated with miR-27b agomir, miR-27b antagomir, or D-ribofuranosylbenzimidazole (an inhibitor of nuclear factor-E2-related factor 2 [Nrf2]) to determine levels of miR-27b, Nrf2, nuclear factor kappa-light-chain-enhancer of activated B cells nuclear factor κB (NF-κB), p-NF-κB, and heme oxygenase-1 (HO-1). The levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) in bronchoalveolar lavage fluid (BALF) were determined.The results of luciferase activity suggested that Nrf2 was a target gene of miR-27b. It was indicated that the Nrf2 level decreased in lung tissues from ALI mice. The downregulation of miR-27b decreased the levels of IL-1β, IL-6, and TNF-α in BALF of ALI mice. Downregulated miR-27b increased Nrf2 level, thus enhancing HO-1 level along with reduction of NF-κB level as well as the extent of NF-κB phosphorylation in the lung tissues of the transfected mice. Pathological changes were ameliorated in LPS-reduced mice elicited by miR-27b inhibition. The results of this study demonstrate that downregulated miR-27b couldenhance Nrf2 and HO-1 expressions, inhibit NF-κB signaling pathway, which exerts a protective effect on LPS-induced ALI in mice.

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Section: Discussionsupporting

confidence: 91%

Downregulated microRNA‐27b attenuates lipopolysaccharide‐induced acute lung injury via activation of NF‐E2‐related factor 2 and inhibition of nuclear factor κB signaling pathway

Huang

Zhu

et al. 2018

Journal Cellular Physiology

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“…Acute lung injury or ALI is a traumatic disease which maybe caused by several direct (shock, severe sepsis, pulmonary contusion, gastroesophageal reflux, pneumonia, drug toxicity, transfusion, and acute pancreatitis) or indirect factors like ventilator induced or mechanical injury etc (Cao et al, 2016). The peculiar characteristics of ALI are enhanced permeability of capillary endothelial and alveolar epithelial cells, scattered pulmonary alveolar and interstitial edema, progressive and refractory hypoxemia and impaired gas exchange all of which expedite arterial hypoxemia,ultimately leading to respiratory failure (Zeng et al, 2013;Tamarapu Parthasarathy et al, 2012;Xie et al, 2012;Cai et al, 2012a;Agarwal et al, 2006).…”

Section: Macrophages In Acute Lung Injurymentioning

confidence: 99%

Macrophages: Their role, activation and polarization in pulmonary diseases

et al. 2018

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Macrophages, circulating in the blood or concatenated into different organs and tissues constitute the first barrier against any disease. They are foremost controllers of both innate and acquired immunity, healthy tissue homeostasis, vasculogenesis and congenital metabolism. Two hallmarks of macrophages are diversity and plasticity due to which they acquire a wobbling array of phenotypes. These phenotypes are appropriately synchronized responses to a variety of different stimuli from either the tissue microenvironment or - microbes or their products. Based on the phenotype, macrophages are classified into classically activated/(M1) and alternatively activated/(M2) which are further sub-categorized into M2a, M2b, M2c and M2d based upon gene expression profiles. Macrophage phenotype metamorphosis is the regulating factor in initiation, progression, and termination of numerous inflammatory diseases. Several transcriptional factors and other factors controlling gene expression such as miRNAs contribute to the transformation of macrophages at different points in different diseases. Understanding the mechanisms of macrophage polarization and modulation of their phenotypes to adjust to the micro environmental conditions might provide us a great prospective for designing novel therapeutic strategy. In view of the above, this review summarises the activation of macrophages, the factors intricated in activation along with benefaction of macrophage polarization in response to microbial infections, pulmonary toxicity, lung injury and other inflammatory diseases such as chronic obstructive pulmonary dysplasia (COPD), bronchopulmonary dysplasia (BPD), asthma and sepsis, along with the existing efforts to develop therapies targeting this facet of macrophage biology.

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“…The macrophages are important mediator in both acute and chronic inflammation [15], here we selected this population of immune cells for further investigations. As miRNAs have been reported to serve as novel therapeutic targets in acute lung injury and ARDS [13], we adopted the strategy of miRNA microarray to interrogate the expression profile in ARDS-related inflammatory setting. The comparative study has identified multiple differentially expressed candidate miRNAs in ARDS vs control groups.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to its normal functions, assembling evidences suggest that miRNA are also involved in various pathological conditions such as cardiomyopathies [8], atherosclerosis [9], obesity [10] and cancer [11]. Most importantly, emerging evidences suggest that miRNAs play crucial roles in inflammation responses [12], as well as in acute lung injury and ARDS [13]. …”

Section: Introductionmentioning

confidence: 99%

NF-κB-Induced MicroRNA-211 Inhibits Interleukin-10 in Macrophages of Rats with Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome

Wang

Chen

et al. 2018

Cell Physiol Biochem

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Background/Aims: The present study addressed the potential involvement of microRNAs in acute respiratory distress syndrome (ARDS)-related inflammation and elucidates the underlying molecular mechanism. Methods: ARDS rat model was established by lipopolysaccharide, with compromised gas exchange capacity and lung edema. The inflammatory cells from bronchoalveolar lavage fluid (BALF) were profiled with automatic blood cell analyzer. The relative fluorescence intensity of BALF-derived macrophages was analyzed by flow cytometry. The relative microRNA expression was determined using microarray and Taqman assay. The secretory interleukin (IL)-10 was measured by enzyme-linked immunosorbent assay. Luciferase reporter assay was performed to determine the regulatory effects of miR-211 and NF-κB on IL-10 and miR-211 expressions, respectively. Chromatin immunoprecipitation (ChIP) was conducted to detect the direct binding of NK-κB on miR-211 promoter. The protein level was determined by Western blot. Results: The provoked acute inflammation was characterized with increased total cells, macrophages, neutrophils and lymphocytes. The relative expression of miR-211 was aberrantly up-regulated in BALF-derived macrophages from ARDS rats, which was accompanied with reduction of secretory IL-10. We further demonstrated that miR-211 inhibited IL-10 expression by binding to its 3’-UTR. The expression of miR-211 was modulated by NF-κB. Conclusion: Here we elucidated a crucial role of NF-κB/miR-211/IL-10 signaling axis in ARDS-related inflammation.

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MicroRNAs: Novel regulatory molecules in acute lung injury/acute respiratory distress syndrome

Cited by 42 publications

References 41 publications

Downregulated microRNA‐27b attenuates lipopolysaccharide‐induced acute lung injury via activation of NF‐E2‐related factor 2 and inhibition of nuclear factor κB signaling pathway

Downregulated microRNA‐27b attenuates lipopolysaccharide‐induced acute lung injury via activation of NF‐E2‐related factor 2 and inhibition of nuclear factor κB signaling pathway

Macrophages: Their role, activation and polarization in pulmonary diseases

NF-κB-Induced MicroRNA-211 Inhibits Interleukin-10 in Macrophages of Rats with Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome

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