Long non‑coding maternally expressed gene 3 regulates cigarette smoke extract‑induced apoptosis, inﬂammation and cytotoxicity by sponging miR‑181a‑2‑3p in 16HBE cells

Fan, Shiming; Ren, Yan; Zhang, Wenli; Zhang, Huawei; Wang, Cheng

doi:10.3892/ol.2020.12306

Cited by 13 publications

(13 citation statements)

References 49 publications

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“…MEG3 is a lncRNA highly expressed in bronchial epithelial cells which is regulated by the smoke extraction, sponge binding to miR-181a-2-3, leading to higher cell apoptosis and inflammation. 55 Since lnc RP11-86H7.1 interacted with miR-9-5p through a ceRNA mechanism, which would lower miR-9-suppression 5p's of NFKB1 production in bronchial epithelial cells, Zhao and colleagues hypothesized that such ternary network may boost PM2.5 related COPD. 56 Increasing studies have shown that lncRNAs and miRNAs may be closely related to the occurrence and development of COPD, could be potential biomarkers and therapeutics.…”

Section: Copdmentioning

confidence: 99%

“…When cigarette smoke is applied to cells in vitro, it can cause cytotoxicity and an immunological response. MEG3 is a lncRNA highly expressed in bronchial epithelial cells which is regulated by the smoke extraction, sponge binding to miR‐181a‐2‐3, leading to higher cell apoptosis and inflammation 55 . Since lnc RP11‐86H7.1 interacted with miR‐9‐5p through a ceRNA mechanism, which would lower miR‐9‐suppression 5p's of NFKB1 production in bronchial epithelial cells, Zhao and colleagues hypothesized that such ternary network may boost PM2.5 related COPD 56 …”

Section: Chronic Lung Inflammatory Diseasesmentioning

confidence: 99%

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Interaction between long noncoding RNA and microRNA in lung inflammatory diseases

Li,

Huang,

Shi

et al. 2024

Immunity Inflam & Disease

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BackgroundNon‐coding RNAs (ncRNAs) are a group of RNAs that cannot synthesize proteins, but are critical in gene expression regulation. Long non‐coding RNAs (lncRNAs) and microRNAs (miRNAs), the two major family members, are intimately involved in controlling immune response, cell proliferation, apoptosis, differentiation and polarization, and cytokine secretion. Their interactions significantly influence lung inflammatory diseases and could be potential therapeutic targets.ObjectivesThe review aims to elucidate the role of ncRNAs, especially the interactions between lncRNA and miRNA in lung diseases, including acute and chronic lung inflammatory diseases, as well as lung cancer. And provide novel insights into disease mechanisms and potential therapeutic methods.MethodsWe conducted a comprehensive review of the latest studies on lncRNA and miRNA in lung inflammatory diseases. Our research involved searching through electronic databases like PubMed, Web of Science, and Scopus.ResultsWe explain the fundamental characteristics and functions of miRNA and lncRNA, their potential interaction mechanisms, and summarize the newly explorations on the role of lncRNA and miRNA interactions in lung inflammatory diseases.ConclusionsNumerous lncRNAs and miRNAs have been found to partipicate in all stages of lung inflammatory diseases. While ncRNA‐based therapies have been validated and developed, there remain challenges in developing more stable and effective drugs for clinical use.

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Section: Copdmentioning

confidence: 99%

Section: Chronic Lung Inflammatory Diseasesmentioning

confidence: 99%

Interaction between long noncoding RNA and microRNA in lung inflammatory diseases

Li,

Huang,

Shi

et al. 2024

Immunity Inflam & Disease

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“…Increasing studies have shown that microRNAs promote the pathogenesis of COPD by regulating the inflammatory response, and miR-181a-2-3p is downregulated in the serum of COPD patients [Kim et al, 2019;Fan et al, 2021]. To investigate whether there existed the same mechanism of miR-181a-5p in the inflammatory response of COPD mice, mice were injected with rAAv-miR-181a-5p via tail veins 1 h prior to COPD model establishment, and the miR-181a-5p levels in BALF and lung tissues of mice were detected by RT-qPCR.…”

Section: Mir-181a-5p Overexpression Attenuated the Inflammatory Respo...mentioning

confidence: 99%

Role and Mechanism of miR-181a-5p in Mice with Chronic Obstructive Pulmonary Disease by Regulating HMGB1 and the NF-κB Pathway

Zhang¹,

Yu²,

Liu³

et al. 2022

Cells Tissues Organs

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Chronic obstructive pulmonary disease (COPD) is a common respiratory disease. This study explored the mechanism of miR-181a-5p in the inflammatory response in COPD mice. COPD mouse models were established by cigarette smoke (CS) exposure following pretreatment with recombinant adeno-associated virus (rAAv)-miR-181a-5p, si-HMGB1 (high mobility group box 1), and NF-κB pathway inhibitor PDTC, respectively. Pathological changes of lung tissues were determined by HE staining. BALF was collected to count total cells, neutrophils and lymphocytes using a Countess II automatic cell counter. Expressions of NE and inflammatory factors (TNF-α, IL-6, IL-8 and IFN-γ) were detected by ELISA. Binding relationship between miR-181a-5p and HMGB1 was predicted on Starbase (http://starbase.sysu.edu.cn/index.php) and validated by dual-luciferase assay. miR-181a-5p expression was detected by RT-qPCR, and expressions of HMGB1, IκBα, p-IκBα were detected by Western blot. The expression level of miR-181a-5p was lower in lung tissues. miR-181a-5p overexpression alleviated inflammatory response and pathological changes of lung tissues in COPD mice, with decreased pulmonary inflammation scores, total cells, neutrophils, and lymphocytes and expressions of NE and inflammatory factors. HMGB1 expression level was increased in COPD mice. miR-181a-5p targeted HMGB1. si-HMGB1 relieved inflammatory responses in COPD mice. NF-κB was activated in COPD mice, evidenced by degraded IκBα and increased p-IκBα level. si-HMGB1 significantly restrained the activation of NF-κB pathway. Briefly, miR-181a-5p targets HMGB1 to inhibit the NF-κB pathway, thus alleviating the inflammatory response in COPD mice.

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“…Exposure to cigarette smoke extract (CSE) can cause an abnormal inflammatory response in the small airways and alveoli, thereby accelerating the apoptosis of bronchial epithelial cells [19]. CSE-treated bronchial epithelial cells are widely used as an in vitro model of COPD [20][21][22]. The normal human bronchial epithelial cell line 16HBE was purchased from American Type Culture Collection (ATCC; USA) and cultured in RPMI-1640 medium (Invitrogen, USA) supplemented with 10% fetal bovine serum (FBS, Invitrogen) at 37 °C with 5% CO 2 .…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

XIST promotes apoptosis and the inflammatory response in CSE-stimulated cells via the miR-200c-3p/EGR3 axis

et al. 2021

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Background Chronic obstructive pulmonary disease (COPD) is a disease that causes obstructed airways and abnormal inflammatory responses in the lungs. Early growth response 3 (EGR3) has been revealed to play a vital role in the regulation of the inflammatory response in certain diseases. We aimed to explore the role of EGR3 and its upstream mechanism in COPD. Methods and result In the present study, 16HBE cells were treated with cigarette smoke extract (CSE) to mimic the inflammatory response in vitro. RT-qPCR revealed that the expression of EGR3 was upregulated in lungs from COPD patients. EGR3 expression in 16HBE cells was increased by CSE treatment. Moreover, flow cytometry analysis and western blot analysis showed that EGR3 downregulation inhibited 16HBE cell apoptosis. EGR3 silencing decreased the protein levels of IL-6, TNF-α, IL-1β and COX2 in CSE-stimulated 16HBE cells. In addition, EGR3 was targeted by microRNA-200c-3p (miR-200c-3p) in 16HBE cells. MiR-200c-3p expression was significantly decreased in lung tissues from COPD patients compared to that in healthy controls. Furthermore, miR-200c-3p bound to lncRNA X-inactive specific transcript (XIST) in 16HBE cells. Additionally, XIST expression was elevated in lung tissues from COPD patients. Rescue assays indicated that EGR3 overexpression counteracted the effects of XIST downregulation on apoptosis and inflammation in CSE-stimulated 16HBE cells. Conclusion The XIST/miR-200c-3p/EGR3 axis facilitated apoptosis and inflammation in CSE-stimulated 16HBE cells. These findings may provide novel insight for treating COPD by alleviating lung inflammation.

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Long non‑coding maternally expressed gene 3 regulates cigarette smoke extract‑induced apoptosis, inﬂammation and cytotoxicity by sponging miR‑181a‑2‑3p in 16HBE cells

Cited by 13 publications

References 49 publications

Interaction between long noncoding RNA and microRNA in lung inflammatory diseases

Interaction between long noncoding RNA and microRNA in lung inflammatory diseases

Role and Mechanism of miR-181a-5p in Mice with Chronic Obstructive Pulmonary Disease by Regulating HMGB1 and the NF-κB Pathway

XIST promotes apoptosis and the inflammatory response in CSE-stimulated cells via the miR-200c-3p/EGR3 axis

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