Citation:Wei M,Chen LM,Huang ZY,Zhang GW,Guan HJ,Ji M.Expression profile analysis to identify potential gene changes induced by dexamethasone in the trabecular meshwork.Int J Ophthalmol 2022;15(8):1240-1248,doi:10.18240/ijo.2022.08.03
Expression profile analysis to identify potential gene changes induced by dexamethasone in the trabecular meshwork
Received:January 26, 2022  Revised:June 17, 2022
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DOI:10.18240/ijo.2022.08.03
Key Words:dexamethasone  trabecular meshwork cells  steroid-induced glaucoma  differentially expressed genes  protein-protein interaction
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AuthorInstitution
Miao Wei Eye Institute, Affiliated Hospital of Nantong University, Nantong , Jiangsu Province, China; Dalian Medical University, Dalian , Liaoning Province, China
Lu-Ming Chen Eye Institute, Affiliated Hospital of Nantong University, Nantong , Jiangsu Province, China
Ze-Yu Huang Eye Institute, Affiliated Hospital of Nantong University, Nantong , Jiangsu Province, China
Guo-Wei Zhang Eye Institute, Affiliated Hospital of Nantong University, Nantong , Jiangsu Province, China
Huai-Jin Guan Eye Institute, Affiliated Hospital of Nantong University, Nantong , Jiangsu Province, China
Min Ji Eye Institute, Affiliated Hospital of Nantong University, Nantong , Jiangsu Province, China
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Abstract:
      AIM: To investigate potential gene changes in trabecular meshwork (TM) induced by dexamethasone (DEX) in steroid-induced glaucoma (SIG).

    METHODS: The expression data of 24 cases from a public functional genomics data were sorted to identify the mechanisms of action of DEX on the TM. The relationships of the differentially expressed genes (DEGs) were enriched using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. In addition, the hub genes were screened by the Search Tool for the Retrieval of Interacting Genes Database (STRING) and Cytoscape tools. Finally, human TM cells (HTMCs) were treated with DEX to preliminarily explore the function of hub genes.

    RESULTS: Totally 47 DEGs, including 21 downregulated and 26 upregulated genes were identified. The primary enriched results of the DEGs consisted of inflammatory response, extracellular matrix (ECM), negative regulation of cell proliferation, TNF signalling pathway and the regulation of tryptophan channels by inflammatory mediators. Subsequently, pro-melanin-enriched hormone (PMCH) and Bradykinin B1 receptor (BDKRB1) were screened as hub genes. It is verified in GSE37474 data set. Western blot and quantitative real-time polymerase chain reaction (qPCR) results showed that protein and RNA expression levels of BDKRB1 were significantly decreased after DEX treatment, while PMCH was not significantly changed.

    CONCLUSION: BDKRB1 may be a key gene involved in SIG onset, providing a suitable therapeutic target for improving the prognosis of SIG patients.

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