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Sodium Propionate Alleviates Atopic Dermatitis by Inhibiting Ferroptosis via Activation of LTBP2/FABP4 Signaling
Anni Xie1, Weijia Li2, Danni Ye1
1Department of Neonatology, Affiliated Women's Hospital of Jiangnan University, Wuxi Maternity and Child Health Care Hospital, Wuxi, 214002, People's Republic of China.
Insights
Sodium propionate (SP) may treat atopic dermatitis (AD) by regulating ferroptosis. This study explored SP’s mechanism in AD, identifying the LTBP2/FABP4 pathway as key to its therapeutic effects.
Area of Science:
- Dermatology
- Molecular Biology
- Computational Biology
Background:
- Atopic dermatitis (AD) is a prevalent pediatric skin condition.
- Emerging evidence suggests ferroptosis plays a role in AD pathogenesis.
- The therapeutic mechanism of sodium propionate (SP) in AD, particularly its effect on ferroptosis, requires elucidation.
Purpose of the Study:
- To investigate whether SP alleviates AD by modulating ferroptosis-related pathways.
- To utilize bioinformatic and in vitro analyses to uncover SP's mechanism of action in AD.
- To identify key genes and pathways involved in SP's therapeutic effects on AD.
Main Methods:
- Analysis of a public AD gene expression dataset (GEO cohort GSE107361).
- Compilation of ferroptosis-related genes and SP target genes.
- Application of Gene Set Variation Analysis (GSVA), Gene Ontology (GO), KEGG, and Weighted Gene Co-expression Network Analysis (WGCNA).
- Establishment of TNF-α/IFN-γ induced AD cell models (HaCat cells) for in vitro validation.
Main Results:
- Ferroptosis-related genes effectively distinguished between healthy controls and AD patients.
- Key AD-associated gene modules and potential SP therapeutic targets were identified.
- Cyclin-dependent kinase 1 (CDK1), latent transforming growth factor beta binding protein 2 (LTBP2), and fatty acid binding protein 4 (FABP4) were highlighted as significant genes.
- SP treatment in vitro increased the expression of skin barrier genes loricrin (LOR) and filaggrin (FLG).
Conclusions:
- SP demonstrates potential in alleviating AD symptoms.
- The therapeutic effects of SP in AD appear to be mediated through the modulation of ferroptosis.
- The LTBP2/FABP4 pathway is implicated as a crucial mechanism in SP's action against AD.
Background:
Atopic dermatitis (AD) is a common pediatric skin disease, with recent studies suggesting a role for ferroptosis in its pathogenesis. Sodium propionate (SP) has shown therapeutic potential in AD, yet its mechanism, particularly regarding ferroptosis modulation, remains unclear. This study aims to explore whether SP alleviates AD by modulating ferroptosis-related pathways through bioinformatic and in vitro analyses.
Methods:
We analyzed the GEO AD cohort (GSE107361). Ferroptosis-related genes was compiled from the GeneCards Database and SP-associated therapeutic target genes were obtained from Swiss Target Prediction. To explore potential biological mechanisms, we employed Gene Set Variation Analysis (GSVA), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Weighted Gene Co-expression Network Analysis (WGCNA) and differential expression analysis identified key gene modules. We also established TNF-α/IFN-γ induced AD cell models using HaCat cells and collected cell samples for further experiments.
Results:
The GSVA analysis demonstrated that ferroptosis-related genes could differentiate between healthy children and those with AD. The identified module includes genes with correlated expression patterns specifically linked to AD. Analysis using three algorithms identified potential therapeutic targets of SP. We screened 51 key genes related to AD and ferroptosis, selecting cyclin-dependent kinase 1 (CDK1) and latent transforming growth factor beta binding protein 2 (LTBP2) as co-expressed genes. Machine learning identified fatty acid binding protein 4 (FABP4) as a significant gene intersection of the 51 key genes. The bioinformatics analysis results were validated through cell experiments, showing that SP treatment increased the expression of the damaged skin genes loricrin (LOR) and filaggrin (FLG).
Conclusion:
Our study indicates that SP may alleviate AD symptoms by modulating ferroptosis through the LTBP2/FABP4 pathway.
