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Related Experiment Video

Updated: Sep 10, 2025

Visualizing Genetic Variants, Short Targets, and Point Mutations in the Morphological Tissue Context with an RNA In Situ Hybridization Assay
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RNA Sequencing Provides Insight Into Idiopathic Subglottic Stenosis.

Mursalin M Anis1, Anthony J Griswold2, Ahmed M S Soliman3

  • 1Department of Otolaryngology, University of Miami Miller School of Medicine, Miami, Florida, USA.

The Laryngoscope
|August 19, 2025
PubMed
Summary
This summary is machine-generated.

Idiopathic subglottic stenosis (iSGS) involves epithelial-mesenchymal transition (EMT) as a key upregulated pathway. Inflammatory pathways are more prominent in post-intubation stenosis, with IL-17 signaling important in both conditions.

Keywords:
RNA sequencingepithelial‐mesenchymal transitionidiopathic subglottic stenosislaryngotracheal stenosis

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Area of Science:

  • Laryngology and Otolaryngology
  • Molecular Biology
  • Genomics

Background:

  • Idiopathic subglottic stenosis (iSGS) is a rare condition affecting the airway below the vocal cords.
  • Understanding the molecular mechanisms of iSGS is crucial for developing targeted therapies.
  • Previous studies suggest a role for inflammation, but specific gene expression profiles remain underexplored.

Purpose of the Study:

  • To determine differential gene expression in idiopathic subglottic stenosis (iSGS).
  • To identify key molecular pathways involved in the pathogenesis of iSGS.
  • To compare gene expression profiles between iSGS and post-intubation laryngotracheal stenosis (iLTS).

Main Methods:

  • RNA sequencing (RNAseq) was performed on subglottic and tracheal tissues from 19 patients (11 iSGS, 8 iLTS).
  • Differential gene expression analysis was conducted using DESeq2.
  • Bioinformatic approaches, including Gene Set Enrichment Analysis (GSEA) and Gene Ontology, were employed to identify significant pathways.

Main Results:

  • 68 differentially expressed genes (DEGs) were identified between iSGS and iLTS (female cohorts).
  • Epithelial-mesenchymal transition (EMT) was the most upregulated pathway in iSGS.
  • TNFα signaling via NF-κB was the most downregulated pathway in iSGS; IL-17 signaling was enriched.
  • Cell-cell adhesion and neutrophil aggregation pathways were significant among candidate DEGs.

Conclusions:

  • EMT is a significant upregulated pathway in iSGS pathogenesis.
  • Inflammatory pathways are more pronounced in iLTS compared to iSGS.
  • IL-17 signaling is implicated in both iSGS and iLTS, while the role of innate immunity requires further investigation.