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Article

MicroRNA-181b stimulates inflammation via the nuclear factor-κB signaling pathway in vitro

  • Authors:
    • Yazhen Wang
    • Genxiang Mao
    • Yuandong Lv
    • Qingdong Huang
    • Guofu Wang
  • View Affiliations / Copyright

    Affiliations: Zhejiang Provincial Key Laboratory of Geriatrics and Geriatrics Institute of Zhejiang, Zhejiang Hospital, Hangzhou, Zhejiang 310013, P.R. China
  • Pages: 1584-1590
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    Published online on: August 24, 2015
       https://doi.org/10.3892/etm.2015.2702
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Abstract

Acute lung injury (ALI) is characterized by severe lung edema and an increase in the inflammatory reaction. Considerable evidence has indicated that microRNAs (miRNAs or miRs) are involved in various human diseases; however, the expression profile and function of miRNAs in ALI have been rarely reported. The present study used miRNA microarray and reverse transcription‑quantitative polymerase chain reaction to demonstrate that miR‑181b is the one of the most significantly upregulated miRNA after lipopolysaccharide (LPS) stimulation in human bronchial epithelial cells, BEAS‑2B. To elaborate the role of miR‑181b in ALI, an assay was performed to investigate the overexpression of miR‑181b in BEAS‑2B cells, and the expression of inflammatory factors was then analyzed. The overexpression of miR‑181b resulted in the induction of an increment in interleukin (IL)‑6 levels. p65 was identified to be a primary component of NF‑κB, since it was upregulated in the miR‑181b overexpression in the BEAS‑2B cells, while pyrrolidine dithiocarbamate, a specific inhibitor of NF‑κB, was found to be able to abrogate the upregulation of the expression of p65. In conclusion, the findings of the present study suggested that miR‑181b may be involved in the process of LPS‑induced inflammation in BEAS‑2B cells by activating the NF‑κB signaling pathway, which implies that it may serve as a potential therapeutic target for ALI.
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Copy and paste a formatted citation
Spandidos Publications style
Wang Y, Mao G, Lv Y, Huang Q and Wang G: MicroRNA-181b stimulates inflammation via the nuclear factor-κB signaling pathway in vitro. Exp Ther Med 10: 1584-1590, 2015.
APA
Wang, Y., Mao, G., Lv, Y., Huang, Q., & Wang, G. (2015). MicroRNA-181b stimulates inflammation via the nuclear factor-κB signaling pathway in vitro. Experimental and Therapeutic Medicine, 10, 1584-1590. https://doi.org/10.3892/etm.2015.2702
MLA
Wang, Y., Mao, G., Lv, Y., Huang, Q., Wang, G."MicroRNA-181b stimulates inflammation via the nuclear factor-κB signaling pathway in vitro". Experimental and Therapeutic Medicine 10.4 (2015): 1584-1590.
Chicago
Wang, Y., Mao, G., Lv, Y., Huang, Q., Wang, G."MicroRNA-181b stimulates inflammation via the nuclear factor-κB signaling pathway in vitro". Experimental and Therapeutic Medicine 10, no. 4 (2015): 1584-1590. https://doi.org/10.3892/etm.2015.2702
Copy and paste a formatted citation
x
Spandidos Publications style
Wang Y, Mao G, Lv Y, Huang Q and Wang G: MicroRNA-181b stimulates inflammation via the nuclear factor-κB signaling pathway in vitro. Exp Ther Med 10: 1584-1590, 2015.
APA
Wang, Y., Mao, G., Lv, Y., Huang, Q., & Wang, G. (2015). MicroRNA-181b stimulates inflammation via the nuclear factor-κB signaling pathway in vitro. Experimental and Therapeutic Medicine, 10, 1584-1590. https://doi.org/10.3892/etm.2015.2702
MLA
Wang, Y., Mao, G., Lv, Y., Huang, Q., Wang, G."MicroRNA-181b stimulates inflammation via the nuclear factor-κB signaling pathway in vitro". Experimental and Therapeutic Medicine 10.4 (2015): 1584-1590.
Chicago
Wang, Y., Mao, G., Lv, Y., Huang, Q., Wang, G."MicroRNA-181b stimulates inflammation via the nuclear factor-κB signaling pathway in vitro". Experimental and Therapeutic Medicine 10, no. 4 (2015): 1584-1590. https://doi.org/10.3892/etm.2015.2702
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