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Background <p>The pathogenesis of allergic rhinitis (AR) is affected by a combination of genetic and environmental factors.</p> Objectives <p>This study aimed to investigate the potential mechanisms of long non-coding RNA GATA binding protein 3 antisense RNA 1 (GATA3-AS1) in AR.</p> Materials and methods <p>110 AR patients and 110 healthy controls were enrolled. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR), cell counting kit-8 (CCK-8), flow cytometry, and enzyme-linked immunosorbent assay (ELISA) were employed to measure the GATA3-AS1 expression and function in AR. RNA immunoprecipitation (RIP) and dual-luciferase assays were conducted to investigate the targeting relationships.</p> Results <p>GATA3-AS1 expression was significantly upregulated in children with AR. In this exploratory cohort, GATA3-AS1 exhibited potential diagnostic value for AR. However, this finding was derived from a single cohort without external validation and required confirmation in independent studies. In cellular models, interleukin-13 stimulation induced GATA3-AS1 expression. Knockdown of GATA3-AS1 effectively reversed IL-13-mediated suppression of cell proliferation and promotion of apoptosis. In HNEPC–PBMC co-cultures, it significantly attenuated the upregulation of IgE and interleukin-4 (produced by PBMCs) and restored the expression of anti-inflammatory cytokines such as interleukin-10 and transforming growth factor-β1 (TGF-β1) in HNEPCs. Mechanistically, inhibition of miR-488-3p partially reversed the therapeutic effects of GATA3-AS1 knockdown, while nuclear factor I/A gene (NFIA) silencing partially attenuated the effects of miR-488-3p inhibition on AR.</p> Conclusion <p>The GATA3-AS1/miR-488-3p/NFIA axis may be involved in the pathogenesis of AR based on correlational human data and in vitro mechanistic studies. Further in vivo validation was required to establish causality and assess translational relevance.</p>

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LncRNA GATA3-AS1 promotes allergic rhinitis by regulating the miR-488-3p/NFIA axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月15日

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  • Xin Zhang,
  • Taotao Lu,
  • Rui Li

摘要

Background

The pathogenesis of allergic rhinitis (AR) is affected by a combination of genetic and environmental factors.

Objectives

This study aimed to investigate the potential mechanisms of long non-coding RNA GATA binding protein 3 antisense RNA 1 (GATA3-AS1) in AR.

Materials and methods

110 AR patients and 110 healthy controls were enrolled. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR), cell counting kit-8 (CCK-8), flow cytometry, and enzyme-linked immunosorbent assay (ELISA) were employed to measure the GATA3-AS1 expression and function in AR. RNA immunoprecipitation (RIP) and dual-luciferase assays were conducted to investigate the targeting relationships.

Results

GATA3-AS1 expression was significantly upregulated in children with AR. In this exploratory cohort, GATA3-AS1 exhibited potential diagnostic value for AR. However, this finding was derived from a single cohort without external validation and required confirmation in independent studies. In cellular models, interleukin-13 stimulation induced GATA3-AS1 expression. Knockdown of GATA3-AS1 effectively reversed IL-13-mediated suppression of cell proliferation and promotion of apoptosis. In HNEPC–PBMC co-cultures, it significantly attenuated the upregulation of IgE and interleukin-4 (produced by PBMCs) and restored the expression of anti-inflammatory cytokines such as interleukin-10 and transforming growth factor-β1 (TGF-β1) in HNEPCs. Mechanistically, inhibition of miR-488-3p partially reversed the therapeutic effects of GATA3-AS1 knockdown, while nuclear factor I/A gene (NFIA) silencing partially attenuated the effects of miR-488-3p inhibition on AR.

Conclusion

The GATA3-AS1/miR-488-3p/NFIA axis may be involved in the pathogenesis of AR based on correlational human data and in vitro mechanistic studies. Further in vivo validation was required to establish causality and assess translational relevance.