Allergy, Asthma & Clinical Immunology (Aug 2022)

miR-3934 regulates the apoptosis and secretion of inflammatory cytokines of basophils via targeting RAGE in asthma

  • Liyan Dou,
  • Wenyu Wang,
  • Junwei Wang,
  • Xiaofei Zhang,
  • Xiaoman Hu,
  • Weili Zheng,
  • Kaiyu Han,
  • Guangyou Wang

DOI
https://doi.org/10.1186/s13223-022-00704-z
Journal volume & issue
Vol. 18, no. 1
pp. 1 – 12

Abstract

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Abstract Background Several miRNAs are now known to have clear connections to the pathogenesis of asthma. The present study focused on the potential role of miR-3934 during asthma development. Methods miR-3934 was detected as a down-regulated miRNA in basophils by sequencing analysis. Next, the expression levels of miR-3934 in peripheral blood mononuclear cells of 50 asthma patients and 50 healthy volunteers were examined by RT-qPCR methods. The basophils were then treated with AGEs and transfected with miR-3934 mimics. The apoptosis levels were examined by flow cytometry assay; and the expression levels of cytokines were detected using the ELISA kits. Finally, the Western blot was performed to examined the expression of key molecules in the TGF-β/Smad signaling pathway. Results miR-3934 was down-regulated in the basophils of asthmatic patients. The expression of the pro-inflammatory cytokines IL-6, IL-8 and IL-33 was enhanced in basophils from asthmatic patients, and this effect was partially reversed by transfection of miR-3934 mimics. Furthermore, receiver operating characteristics analysis showed that miR-3934 levels can be used to distinguish asthma patients from healthy individuals. miR-3934 partially inhibited advanced glycation end products-induced increases in basophil apoptosis by suppressing expression of RAGE. Conclusion Our results indicate that miR-3934 acts to mitigate the pathogenesis of asthma by targeting RAGE and suppressing TGF-β/Smad signaling.

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