Anti-inflammatory role of microRNA let-7c in LPS treated alveolar macrophages by targeting STAT3

Yu, Jihui; Li, Long; Luo, Zhixiao; Li, Lin-Man; You, Jie-Ru

doi:10.1016/j.apjtm.2015.12.015

Cited by 25 publications

(19 citation statements)

References 20 publications

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“…Let‐7i can regulate SOCS1 and is critical for endotoxin‐induced immune function . Overexpression of miRNA let‐7c inhibited the production of TNF‐ α , IL‐6, and IL‐1β induced by endotoxin through inhibiting the phosphorylation of STAT3 . The studies have shown that miR‐132, miR‐212, miR‐146b, miR‐155, miR‐200b, miR‐200c, miR‐149, and miR‐203 bind to MyD88 mediating the regulation of TLR4 signaling pathway .…”

Section: The Molecular Mechanisms Of Endotoxin Tolerancementioning

confidence: 99%

Recent advances in endotoxin tolerance

Liú

Cao

Zhou

et al. 2018

J of Cellular Biochemistry

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Endotoxin tolerance is defined as a reduced capacity of a cell to respond endotoxin (lipopolysaccharide, LPS) challenge after an initial encounter with endotoxin in advance. The body becomes tolerant to subsequent challenge with a lethal dose of endotoxin and cytokines release and cell/tissue damage induced by inflammatory reaction are significantly reduced in the state of endotoxin tolerance. The main characteristics of endotoxin tolerance are downregulation of inflammatory mediators such as tumor necrosis factor α (TNF‐α), interleukin‐1β (IL‐1β), and C‐X‐C motif chemokine 10 (CXCL10) and upregulation of anti‐inflammatory cytokines such as IL‐10 and transforming growth factor β (TGF‐β). Therefore, endotoxin tolerance is often regarded as the regulatory mechanism of the host against excessive inflammation. Endotoxin tolerance is a complex pathophysiological process and involved in multiple cellular signal pathways, receptor alterations, and biological molecules. However, the exact mechanism remains elusive up to date. To better understand the underlying cellular and molecular mechanisms of endotoxin tolerance, it is crucial to investigate the comprehensive cellular signal pathways, signaling proteins, cell surface molecules, proinflammatory and anti‐inflammatory cytokines, and other mediators. Endotoxin tolerance plays an important role in reducing the mortality of sepsis, endotoxin shock, and other endotoxin‐related diseases. Recent reports indicated that endotoxin tolerance is also related to other diseases such as cystic fibrosis, acute coronary syndrome, liver ischemia‐reperfusion injury, and cancer. The aim of this review is to discuss the recent advances in endotoxin tolerance mainly based on the cellular and molecular mechanisms by outline the current state of the knowledge of the involvement of the toll‐like receptor 4 (TLR4) signaling pathways, negative regulate factor, microRNAs, apoptosis, chromatin modification, and gene reprogramming of immune cells in endotoxin tolerance. We hope to provide a new idea and scientific basis for the rational treatment of endotoxin‐related diseases such as endotoxemia, sepsis, and endotoxin shock clinically.

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Section: The Molecular Mechanisms Of Endotoxin Tolerancementioning

confidence: 99%

Recent advances in endotoxin tolerance

Liú

Cao

Zhou

et al. 2018

J of Cellular Biochemistry

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“…Therefore, more light needs to be shed on the molecular programmers that drive these functional differences and conclude whether these are observed in a fraction of the AM population. To this end, microRNAs have been involved in the regulation of proinflammatory cytokine release by AMs [ 159 ], whereas recent investigation into the epigenetic networks active in macrophage populations of patients with COPD and healthy smokers revealed that the histone deacetylases HDAC2 and HDAC3 are downregulated in comparison with healthy individuals and correlate negatively with disease severity [ 160 , 161 ]. Similarly, Yang et al showed that oxidative stress induces posttranslational modifications on HDAC2 which are responsible for the loss of function of this enzyme's activity [ 162 ].…”

Section: Ams In Copdmentioning

confidence: 99%

Dysregulated Functions of Lung Macrophage Populations in COPD

Kapellos

Baßler

Aschenbrenner

et al. 2018

Journal of Immunology Research

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Chronic obstructive pulmonary disease (COPD) is a diverse respiratory disease characterised by bronchiolitis, small airway obstruction, and emphysema. Innate immune cells play a pivotal role in the disease's progression, and in particular, lung macrophages exploit their prevalence and strategic localisation to orchestrate immune responses. To date, alveolar and interstitial resident macrophages as well as blood monocytes have been described in the lungs of patients with COPD contributing to disease pathology by changes in their functional repertoire. In this review, we summarise recent evidence from human studies and work with animal models of COPD with regard to altered functions of each of these myeloid cell populations. We primarily focus on the dysregulated capacity of alveolar macrophages to secrete proinflammatory mediators and proteases, induce oxidative stress, engulf microbes and apoptotic cells, and express surface and intracellular markers in patients with COPD. In addition, we discuss the differences in the responses between alveolar macrophages and interstitial macrophages/monocytes in the disease and propose how the field should advance to better understand the implications of lung macrophage functions in COPD.

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“…Both miR21 and miR-181a are involved in chronic systemic inflammation (108) and have been reported to be affected by smoking in humans (109). Cross-sectional studies assessing the sputum of smokers and non-smokers identified let-7c as over-expressed and inversely correlated with tumor necrosis factor receptor type II, implicated in COPD and inflammation pathogenesis and a predicted target gene of let-7c) was inversely correlated with the sputum levels of let-7c (29, 110, 111), and alveolar macrophages alter expression of miR-210, miR-150, miR-146b-3p, and miR-452 (112). The latter miRNA targets matrix metalloproteinase-12, which is increased in the sputum of patients with COPD and contributes the development of emphysema (113, 114).…”

Section: Introductionmentioning

confidence: 99%

A Review of Pulmonary Toxicity of Electronic Cigarettes in the Context of Smoking: A Focus on Inflammation

Shields

Berman

Brasky

et al. 2017

Cancer Epidemiology, Biomarkers &Amp; Prevention

110

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The use of electronic cigarettes (e-cigs) is increasing rapidly, but their effects on lung toxicity are largely unknown. Smoking is a well-established cause of lung cancer and respiratory disease, in part through inflammation. It is plausible that e-cig use might affect similar inflammatory pathways. E-cigs are used by some smokers as an aid for quitting or smoking reduction, and by never smokers (e.g., adolescents and young adults). The relative effects for impacting disease risk may differ for these groups. Cell culture and experimental animal data indicate that e-cigs have the potential for inducing inflammation, albeit much less than smoking. Human studies show that e-cig use in smokers is associated with substantial reductions in blood or urinary biomarkers of tobacco toxicants when completely switching and somewhat for dual use. However, the extent to which these biomarkers are surrogates for potential lung toxicity remains unclear. The FDA now has regulatory authority over e-cigs and can regulate product and e-liquid design features such as nicotine content and delivery, voltage, e-liquid formulations, and flavors. All of these factors may impact pulmonary toxicity. This review summarizes current data on pulmonary inflammation related to both smoking and e-cig use, with a focus on human lung biomarkers.

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Anti-inflammatory role of microRNA let-7c in LPS treated alveolar macrophages by targeting STAT3

Abstract: MiRNA let-7c low expression in COPD can regulate inflammatory responses by targeting STAT3 in alveolar macrophage, which may provide a new target for COPD treatment strategies.

Cited by 25 publications

References 20 publications

Recent advances in endotoxin tolerance

Recent advances in endotoxin tolerance

Dysregulated Functions of Lung Macrophage Populations in COPD

A Review of Pulmonary Toxicity of Electronic Cigarettes in the Context of Smoking: A Focus on Inflammation

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