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Time-dependent Glucocorticoid-Induced Transcriptomic Changes in Human Trabecular Meshwork and Schlemm's Canal.

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Dexamethasone (DEX) alters gene expression in trabecular meshwork and Schlemm

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Area of Science:

  • Ocular biology
  • Transcriptomics
  • Glaucoma research

Background:

  • Glucocorticoids, like dexamethasone (DEX), are widely used but can cause ocular hypertension.
  • The molecular mechanisms underlying DEX-induced ocular hypertension in the trabecular meshwork (TM) and Schlemm's canal endothelial (SCE) cells are not fully understood.

Purpose of the Study:

  • To investigate the transcriptomic alterations induced by DEX in human TM and SCE cells using RNA-sequencing (RNA-seq).
  • To identify genes and pathways involved in DEX-induced changes relevant to intraocular pressure (IOP) and primary open-angle glaucoma (POAG).

Main Methods:

  • Human TM (n=10) and SCE (n=5) cell strains were treated with DEX (100nM) or vehicle for 1 hour, 6 hours, and 2 days.
  • RNA-sequencing was performed, and differential gene expression analysis was conducted using DESeq2.
  • Gene-set enrichment analysis and association testing with POAG and IOP were performed on differentially expressed genes (DEGs).

Main Results:

  • After 2-day DEX exposure, 857 DEGs were identified in TM cells and 2,086 in SCE cells.
  • 411 genes were differentially expressed in both cell types, including significant upregulation of FKBP5 and FAM107A.
  • DEGs were enriched in pathways related to cell adhesion, extracellular matrix, and immune response; early response genes were linked to immune processes.

Conclusions:

  • This study identifies key genes and pathways responsive to DEX in TM and SCE cells, providing insights into glucocorticoid-induced ocular hypertension.
  • Candidate genes, such as LTBP2 and FAM105A, associated with IOP and POAG risk, were identified.
  • The findings offer potential targets for future human genetic analyses related to ocular hypertension.