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G0S2 regulates innate immunity in Kawasaki disease via lncRNA HSD11B1-AS1

Mako Okabe1, Shinya Takarada1, Nariaki Miyao1

  • 1Department of Pediatrics, Faculty of Medicine, University of Toyama, Toyama, Japan.

Pediatric Research
|March 16, 2022
PubMed

Insights

This study investigated long non-coding RNAs (lncRNAs) in Kawasaki disease (KD) inflammation. Researchers identified G0S2 and HSD11B1-AS1 as key molecules involved in KD, suggesting lncRNAs as potential diagnostic targets.

Area of Science:

  • Immunology
  • Genetics
  • Molecular Biology

Background:

  • Kawasaki disease (KD) is a leading cause of acquired heart disease in children, with an unknown etiology.
  • Long non-coding RNAs (lncRNAs) are implicated in various disease pathologies.
  • The role of lncRNAs in KD inflammation requires further investigation.

Purpose of the Study:

  • To investigate the role of lncRNAs in Kawasaki disease inflammation.
  • To identify specific lncRNAs and genes associated with KD pathogenesis.
  • To explore potential diagnostic markers for KD.

Main Methods:

  • Cap analysis gene expression sequencing was performed on monocytes from 50 KD patients.
  • Transcriptome and gene ontology analyses were conducted to identify differentially expressed genes.
  • In vitro experiments using THP-1 monocytes were used to validate findings.

Main Results:

  • Twenty-one candidate lncRNA transcripts were identified, indicating immune system involvement in KD.
  • G0/G1 switch gene 2 (G0S2) and its antisense lncRNA, HSD11B1-AS1, were significantly upregulated during acute KD.
  • Silencing G0S2 reduced HSD11B1-AS1 and tumor necrosis factor-α expression in lipopolysaccharide-induced THP-1 monocytes.

Conclusions:

  • lncRNAs play a critical role in the innate immune response during acute Kawasaki disease.
  • G0S2 and HSD11B1-AS1 are identified as key molecules associated with KD inflammation.
  • lncRNAs represent a promising novel target for KD diagnosis.
Abstract

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