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Potential Genes and Mechanisms Linking Intracerebral Hemorrhage and Depression: A Bioinformatics-Based Study
Cuihua Zou1,2, Xiaohua Huang1,2, Xuequn Lan1
1Department of Neurology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, 533000, People's Republic of China.
Insights
This study identified key genes and pathways involved in post-intracerebral hemorrhage depression. These findings offer insights into the mechanisms of depression following brain hemorrhage.
Area of Science:
- Neuroscience
- Genomics
- Bioinformatics
Background:
- Depression following intracerebral hemorrhage (ICH) is a significant clinical concern.
- The underlying pathogenic mechanisms of post-ICH depression remain incompletely understood.
Purpose of the Study:
- To investigate the potential pathogenic mechanisms of post-intracerebral hemorrhage depression.
- To identify key genes and pathways associated with the co-occurrence of ICH and depression.
Main Methods:
- Utilized Gene Expression Omnibus (GEO) database for gene expression profiles of ICH and depression.
- Performed differential gene expression (DEG) analysis, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis.
- Conducted cross-talk analysis and integrated bridge landscape analysis to identify hub bridge genes.
Main Results:
- Identified 131 DEGs common to ICH and depression.
- Discovered 55 GO terms and KEGG pathways related to interacting genes, with 10 each significantly associated with cross-talk.
- Identified 20 hub bridge genes, including HLA-A, HMOX1, and JUN, potentially involved in immune mediation, cell adhesion, and neurotransmitter pathways.
Conclusions:
- Bioinformatics analysis revealed potential hub bridge genes and pathways implicated in post-ICH depression.
- The findings provide a foundation for future research into the pathogenesis of post-ICH depression.
Purpose:
The purpose of this study was to investigate the potential pathogenic mechanisms of post-intracerebral hemorrhage depression.
Methods:
Profiles of gene expression in brain tissue of patients with intracerebral hemorrhage (ICH) or depression were downloaded from the Gene Expression Omnibus (GEO) database. We analyzed differentially expressed genes (DEGs) for the two diseases separately. With these DEGs, we conducted an enrichment analysis based on Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) as well as cross-talk analysis, then we identified hub bridge genes using integrated bridge landscape analysis.
Results:
We found 131 DEGs for interaction between ICH and depression. In the enrichment analysis, we found 55 GO terms and KEGG pathways involving interacting genes of ICH and depression, and 10 GO terms and 10 KEGG pathways most significantly related to cross-talk between ICH and depression. In the integrated bridge landscape analysis, we identified 20 hub bridge genes. In further analysis, we found that hub bridge genes HLA-A, HMOX1, and JUN related to endocytosis, cell adhesion, and phagosomes may exert their effects through the dopamine (DA) system and the serotonergic pathway post-ICH depression. HLA-A may play a role in the occurrence and development of ICH and depression through immune mediation and cell adhesion. HMOX1 and JUN may participate in the mechanism by interacting with HLA-A.
Conclusion:
Through bioinformatics analysis, we identified potential hub bridge genes and pathways related to post-ICH depression. Our study provides references for further research on mechanisms on the pathogenesis of post-ICH depression.
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