Dexmedetomidine targets miR-146a and participates in the progress of chronic obstructive pulmonary disease in vivo and in vitro

Li, Na; Li, Shuangfeng; Wu, Yehua; Xiong, Lei; Li, Tiejun; Xing, Dandan; Li, Qiuchang; Wu, Duozhi

doi:10.1007/s13258-020-01019-2

Cited by 1 publication

(2 citation statements)

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“…As expected, TNF-α treatment increased the mRNA and protein level of MUC5AC in 16HBE cells 1D,E). The previous studies have demonstrated that miR-134-5p (miR-134) and miR-146a-5p (miR-146a) are involved in mucus hypersecretion in COPD (12,(16)(17)(18)(19). To explore the association of TNF-α-induced MUC5AC expression with these miRNAs, we first assessed whether TNF-α regulated the expression of these miRNAs.…”

Section: Tnf-α Treatment Increased Muc5ac Expression and Repressed Mir-134-5p (Mir-134) And Mir-146a-5p (Mir-146a) Expression In 16hbe Cementioning

confidence: 99%

“…miR-134-5p is a potential marker for the clinical diagnose of acute exacerbation of COPD (16). Down-regulated miR-146a-5p is involved in the pathogenesis of COPD through inducing more proinflammatory phenotype (17)(18)(19). Given that NF-κB signaling acts as critical roles in facilitating mucin 5AC (MUC5AC) expression (20) and miR-134-5p possesses a potential effect of regulating NF-κB activation, we thus investigated whether miR-134-5p repressed MUC5AC expression by inhibiting NF-κB signaling in cell model of airway mucus hypersecretion.…”

Section: Introductionmentioning

confidence: 99%

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Tumor necrosis factor-α promotes airway mucus hypersecretion by repressing miR-146a-5p and miR-134-5p levels in human airway epithelial cells

Fu¹,

Zhang²,

Zhang³

et al. 2021

Transl Cancer Res TCR

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Background: Airway mucus acts as an indispensable protective component of innate immune response against invading pathogens. However, airway mucus hypersecretion, largely consisting of mucin 5AC (MUC5AC), is the leading cause of airflow obstruction and airway hyperresponsiveness that contributes to chronic obstructive pulmonary disease (COPD). MicroRNAs (miRNAs) are frequently dysregulated in the pathogenesis of COPD, but the definite role of miRNAs in airway mucus hypersecretion is not well understood.Methods: A cell model of mucus hypersecretion was established in 16HBE cells by treatment with TNF-α.Cell viability and apoptosis were assessed using cell counting kit-8 (CCK-8) and flow cytometry, respectively.The aberrant expression of miR-146a-5p and miR-134-5p was assayed in TNF-α-treated 16HBE cells, and the effect of miR-146a-5p and miR-134-5p on regulating MUC5AC expression was evaluated using quantitative real-time PCR (qPCR) and Western blot analysis.Results: TNF-α treatment resulted in a significant decrease of cell viability, and increase of cell apoptosis and MUC5AC expression in 16HBE cells. Additionally, the expression of miR-134-5p and miR-146a-5p was markedly decreased in the cell model. Importantly, forced expression of miR-134-5p and miR-146a-5p significantly repressed TNF-α-induced upregulation of MUC5AC. Mechanistically, although miR-134-5p did not affect 16HBE cells viability and apoptosis, miR-134-5p partially blocked TNF-α-induced MUC5AC expression by inhibiting the activation of NF-κB signaling. On the other hand, miR-146a-5p enhanced cell viability and reduced cell apoptosis. miR-146a-5p also repressed TNF-α-induced MUC5AC expression by inhibiting p38 MAPK (mitogen-activated protein kinase) signaling activation. Conclusions:The current data demonstrated that both miR-134-5p and miR-146a-5p conferred protection against TNF-α-induced mucus hypersecretion through repressing NF-κB and p38 MAPK signaling, indicating that miR-134-5p and miR-146a-5p may serve as the biomarker for COPD.

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Section: Tnf-α Treatment Increased Muc5ac Expression and Repressed Mir-134-5p (Mir-134) And Mir-146a-5p (Mir-146a) Expression In 16hbe Cementioning

confidence: 99%