Related Experiment Video
Updated: May 6, 2026

11:28
Analytical Techniques for Assaying Nitric Oxide Bioactivity
Published on: June 18, 2012
18.0K
Transcriptome analysis in various cell lines exposed to nitric oxide.
Tohta Mizushima1, Sho Kubota1, Yuta Iijima1
1Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University.
The Journal of Toxicological Sciences
|June 2, 2024
Summary
Chronic nitric oxide (NO) exposure alters gene expression, impacting cell adhesion and inflammation. This study investigates NO
Area of Science:
- Biochemistry
- Molecular Biology
- Toxicology
Background:
- Nitric oxide (NO) is a signaling molecule with physiological roles.
- Excessive or chronic NO acts as an inflammatory mediator and can cause toxic effects.
- NO-induced S-nitrosylation inhibits DNA methyltransferases, potentially altering gene expression and contributing to disease.
Purpose of the Study:
- To investigate the effects of chronic nitric oxide (NO) exposure on the transcriptome.
- To understand how NO influences gene expression in different cell types.
- To elucidate the role of NO in the pathogenesis of NO-associated inflammatory diseases.
Main Methods:
- Transcriptome analysis was performed on A549, AGS, HEK293T, and SW48 cells.
- Cells were exposed to 100 μM nitric oxide (NO) for 48 hours.
- Gene ontology and gene set enrichment analyses were utilized to interpret gene expression changes.
Main Results:
- Differentially expressed genes in response to NO exposure were cell-specific.
- Gene ontology analysis revealed upregulation of genes related to cell adhesion and migration in several cell lines.
- Gene set enrichment analysis indicated that NO stimulated inflammation-related gene expression across various cell lines.
Conclusions:
- Chronic NO exposure significantly alters cellular transcriptomes in a cell-specific manner.
- NO exposure upregulates genes associated with cell adhesion, migration, and inflammation.
- These findings contribute to understanding the molecular mechanisms underlying NO-associated inflammatory diseases.

