Expression profile analysis to identify potential gene changes induced by dexamethasone in the trabecular meshwork

Area of Science:

• Ophthalmology
• Genomics
• Molecular Biology

Background:

• Steroid-induced glaucoma (SIG) is a significant side effect of corticosteroid therapy.
• The trabecular meshwork (TM) plays a crucial role in regulating intraocular pressure.
• Understanding gene expression changes in the TM induced by dexamethasone (DEX) is vital for SIG research.

Purpose of the Study:

• To identify gene expression alterations in the TM caused by DEX.
• To elucidate the molecular mechanisms underlying DEX-induced TM changes.
• To identify potential therapeutic targets for SIG.

Main Methods:

• Analysis of gene expression data from 24 cases.
• Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis.
• Identification of hub genes using STRING and Cytoscape, followed by validation in human TM cells (HTMCs).

Main Results:

• 47 differentially expressed genes (DEGs) were identified, including inflammatory response and extracellular matrix-related genes.
• Pro-melanin-enriched hormone (PMCH) and Bradykinin B1 receptor (BDKRB1) were identified as hub genes.
• BDKRB1 expression was significantly decreased in HTMCs after DEX treatment, while PMCH showed no significant change.

Conclusions:

• BDKRB1 is implicated as a key gene in the pathogenesis of SIG.
• BDKRB1 represents a potential therapeutic target for improving SIG outcomes.
• Further research into BDKRB1's role could lead to novel SIG treatments.