Differential expression of miR‑4492 and IL‑10 is involved in chronic rhinosinusitis with nasal polyps

Li, Linge; Jiang, Feng; Zhang, Dinghao; Yong, Jun; Wang, Yan; Huang, Rongfu

doi:10.3892/etm.2019.8022

Cited by 12 publications

(15 citation statements)

References 56 publications

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“…Studies performed on CRSwNP mainly focus on exploring potential inflammatory factors and targeted therapy [ 17 , 18 ]. Moreover, a previous study showed that miR-4492/IL-10 interaction played a crucial role in CRSwNP [ 19 ]. Xiao et al discovered that IL-21 was highly expressed in CRSwNP groups, and suggested that IL-21 might be a therapeutic target for CRSsNP therapy [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

Let-7a-5p regulates the inflammatory response in chronic rhinosinusitis with nasal polyps

Zhang

Han²,

Chen

2021

Diagn Pathol

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Background Let-7a-5p is demonstrated to be a tumor inhibitor in nasopharyngeal carcinoma. However, the role of let-7a-5p in chronic rhinosinusitis with nasal polyps (CRSwNP) has not been reported. This study is designed to determine the pattern of expression and role of let-7a-5p in CRSwNP. Methods The expression level of let-7a-5p, TNF-α, IL-1β, and IL-6 in CRSwNP tissues and cells were detected by RT-qPCR. Western blot assay was carried out to measure the protein expression of the Ras-MAPK pathway. Dual luciferase reporter assay and RNA pull-down assay were used to explore the relationship between let-7a-5p and IL-6. Results Let-7a-5p was significantly downregulated in CRSwNP tissues and cells. Moreover, the mRNA expression of TNF-α, IL-1β and IL-6 was increased in CRSwNP tissues, while let-7a-5p mimic inhibited the expression of TNF-α, IL-1β and IL-6. Besides that, let-7a-5p was negatively correlated with TNF-α, IL-1β and IL-6 in CRSwNP tissues. In our study, IL-6 was found to be a target gene of let-7a-5p. Additionally, let-7-5p mimic obviously reduced the protein levels of Ras, p-Raf1, p-MEK1 and p-ERK1/2, while IL-6 overexpression destroyed the inhibitory effect of let-7a-5p on the Ras-MAPK pathway in CRSwNP. Conclusion We demonstrated that let-7a-5p/IL-6 interaction regulated the inflammatory response through the Ras-MAPK pathway in CRSwNP.

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Section: Discussionmentioning

confidence: 99%

Let-7a-5p regulates the inflammatory response in chronic rhinosinusitis with nasal polyps

Zhang

Han²,

Chen

2021

Diagn Pathol

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“…Based on the presence or absence of polyposis, CRS can be divided into CRSwNP and CRSsNP ( 5 ). Though the occurrence of CRSwNP is infrequent, medical intervention is unsuccessful for a large proportion of patients with CRSwNP ( 8 ). In addition to inflammation, CRSwNP and CRSsNP are characterized by remodeling of structural components, particularly in the epithelium ( 30 ).…”

Section: Discussionmentioning

confidence: 99%

“…CRSwNP is more closely associated with obstruction of the nasal cavity and anosmia ( 7 ). Clinically, CRSwNP is frequently resistant to medical therapy ( 8 ). Recently, it has been demonstrated that epithelial-to-mesenchymal transition (EMT) and its effects on nasal epithelial cells may result in the tissue remodeling of nasal polyps ( 9 ).…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, miR-142-3p may regulate inflammatory responses by regulating tumor necrosis factor α ( 11 ). Interactions between miR-4492 and interleukin 10 associated with Janus kinase/signal transducers and activators of the transcription signaling pathway may be one of the key mechanisms in CRSwNP ( 8 ). miR-155-5p has also been reported to be targeted by circular RNA nuclear receptor subfamily 1 group H member 4 in the pathological process of renal injury regulation in salt-sensitive hypertensive mice ( 12 ).…”

Section: Introductionmentioning

confidence: 99%

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miR‑155‑5p downregulation inhibits epithelial‑to‑mesenchymal transition by targeting SIRT1 in human nasal epithelial cells

et al. 2020

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epithelial-to-mesenchymal transition (eMT) in nasal epithelial cells is involved with tissue remodeling of nasal polyps. The present study investigated the molecular mechanisms through which mir-155-5p regulated eMT in chronic rhinosinusitis (crS). Patients were divided into the following groups: crSsnP, crS without nasal polyposis group, crSwnP, crS with nasal polyposis and controls. The expression of transforming growth factor (TGF)-β1, eMT markers, sirtuin 1 (SirT1) and mir-155-5p were determined by western blotting and reverse transcription-quantitative Pcr. cell morphology following TGF-β1 treatment in the presence of mir-155-5p inhibitors or controls was observed under a microscope. Target genes and potential binding sites between mir-155-5p and SirT1 were predicted by TargetScan and confirmed using dual-luciferase reporter assay. In patients with crS, the expression levels of e-cadherin were downregulated and the expression levels of TGF-β1, mesenchymal markers and mir-155-5p were upregulated. additionally, these changes in expression levels were reduced or increased to a greater extent in the crSwnP group compared with the crSsnP group. Furthermore, TGF-β1 expression promoted eMT in human nasal epithelial cells (Hnepcs) and upregulated mir-155-5p expression. These effects were reversed by mir-155-5p inhibitors. additionally, SirT1 was predicted as a target gene of mir-155-5p. downregulation of mir-155-5p upregulated epithelial marker expression and downregulated mesenchymal marker expression by regulating SirT1. Therefore, the downregulation of mir-155-5p inhibited eMT in Hnepcs by targeting SirT1.

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“…MicroRNAs (miR) are a class of small noncoding RNAs that regulate the expression of target genes by preventing the translation of target mRNAs or inducing their degradation, or both, depending on the level of complementarity (12). MicroRNAs are involved in the regulation of immune systems and inflammation (13,14), and increasing studies show that miRNAs play an important role in the pathogenesis of NP (15)(16)(17)(18). MiR-21, a member of microRNAs, is highlighted as potentially playing a pivotal role in regulating inflammation (19)(20)(21).…”

Section: Introductionmentioning

confidence: 99%

Elevated microRNA-21 Is a Brake of Inflammation Involved in the Development of Nasal Polyps

Liu

Zhou

et al. 2021

Front. Immunol.

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BackgroundCRSwNP is an inflammatory disease but the mechanism is not yet fully understood. MiR-21, a member of miRNAs, has been reported to play roles in mediating inflammation. However, the expression of miR-21 and its role in patients with CRSwNP remain elusive.MethodsTurbinates from control subjects, uncinate processes from CRSsNP, polyp tissues from CRSwNP, and nasal epithelial cells brushed from nasal mucosa were collected. The expression of miR-21 and cytokines in nasal tissues and epithelial cells were detected by qPCR. The localization of miR-21 was detected by ISH, and its target was identified by bioinformation analysis, qPCR, IHC, WB, and luciferase reporter system. The protein and mRNA of PDCD4 and NF-κB P65 were determined by WB and qPCR after miR-21 transfection in HNEpC. The role of miR-21 on cytokines was analyzed in HNEpC and nasal polyp explants.ResultsMiR-21 was upregulated in CRSwNP relative to control subjects by qPCR, which was determined mainly in nasal epithelial cells of CRSwNP by ISH. Both pro-inflammation cytokines (IL-1β, IL-6, IL-8, IL-25, and TSLP) and a suppressive cytokine (IL-10) were overexpressed in the epithelial cells of CRSwNP. The expression of miR-21 was positively correlated with IL-10 and negatively correlated with IL-6, IL-8, IL-33, and TSLP in the epithelial cells of CRSwNP. As a potential target of miR-21, the expression of PDCD4 was negatively correlated with miR-21 in CRSwNP. In HNEpC, miR-21 could reduce the expression of PDCD4 at both mRNA and protein levels, and bioinformation analysis and luciferase reporter system confirmed PDCD4 as one target of miR-21. Furthermore, miR-21 could decrease the activation of NF-κB and increase IL-10 mRNA. Both SEB and LPS could elevate miR-21, with IL-25, IL-33, TSLP induced by SEB and IL-1β, IL-6, IL-8 induced by LPS, while the miR-21 could regulate the expression of IL-33, TSLP, IL-1β, IL- 6 and IL-8 in vitro and ex vivo. Clinically, miR-21 expression was inversely correlated with the Lund-Mackay CT scores and the Lund-Kennedy scores in CRSwNP.ConclusionMiR-21 could be a prominent negative feedback factor in the inflammation process to attenuate the expression of pro-inflammatory cytokines, thereby playing an anti-inflammation role in CRSwNP.

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Differential expression of miR‑4492 and IL‑10 is involved in chronic rhinosinusitis with nasal polyps

Cited by 12 publications

References 56 publications

Let-7a-5p regulates the inflammatory response in chronic rhinosinusitis with nasal polyps

Let-7a-5p regulates the inflammatory response in chronic rhinosinusitis with nasal polyps

miR‑155‑5p downregulation inhibits epithelial‑to‑mesenchymal transition by targeting SIRT1 in human nasal epithelial cells

Elevated microRNA-21 Is a Brake of Inflammation Involved in the Development of Nasal Polyps

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