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miRNA-302e attenuates inflammation in infantile pneumonia though the RelA/BRD4/NF-κB signaling pathway

Shaoxia Li1, Wenwen Cui1, Qing Song1

  • 1Department of Pediatrics, The People's Hospital of Dongying, Dongying, Shandong 257091, P.R. China.

International Journal of Molecular Medicine
|May 23, 2019
PubMed

Insights

MicroRNA-302e plays a protective role in infantile pneumonia (IP). Its reduced expression exacerbates inflammation, while its overexpression alleviates it by targeting the RelA/BRD4/NF-κB pathway.

Area of Science:

  • Molecular Biology
  • Immunology
  • Pediatric Medicine

Background:

  • Infantile pneumonia (IP) is a significant pediatric respiratory illness.
  • The molecular mechanisms underlying IP pathogenesis require further elucidation.
  • MicroRNAs (miRNAs) are emerging as key regulators in inflammatory diseases.

Purpose of the Study:

  • To investigate the role of microRNA (miRNA)-302e in infantile pneumonia (IP).
  • To explore the protective mechanisms of miRNA-302e in IP.
  • To identify the signaling pathway involved in miRNA-302e's effect on IP.

Main Methods:

  • Utilized a mouse model of IP to assess miRNA-302e expression.
  • Employed in vitro models of IP to study the effects of miRNA-302e manipulation.
  • Administered anti-miRNA-302e and overexpressed miRNA-302e.
  • Used small interfering RNAs (siRNAs) targeting RelA, BRD4, and NF-κB.

Main Results:

  • miRNA-302e expression was found to be reduced in a mouse model of IP.
  • Administration of anti-miRNA-302e increased inflammation and induced RelA, BRD4, and NF-κB protein expression in vitro.
  • Overexpression of miRNA-302e reduced inflammation and suppressed RelA, BRD4, and NF-κB protein expression in vitro.
  • si-RelA, si-BRD4, or si-NF-κB attenuated the effects of miRNA-302e on inflammation.

Conclusions:

  • miRNA-302e exhibits a protective role in infantile pneumonia.
  • miRNA-302e attenuates inflammation in IP by regulating the RelA/BRD4/NF-κB signaling pathway.

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