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CREB3L1 Modulates Extracellular Matrix Gene Expression and Proliferation in Glaucomatous Lamina Cribrosa Cells
Mustapha Irnaten1,2, Ellen Gaynor1, Liam Bourke2
1Clinical Research Centre, School of Medicine, University College Dublin, D04 V1W8 Dublin, Ireland.
Biomedicines
|March 28, 2026
Summary
cAMP responsive element-binding protein 3-like 1 (CREB3L1) is elevated in glaucoma lamina cribrosa cells, driving fibrotic remodeling. Reducing CREB3L1 suppressed extracellular matrix production and cellular activity, suggesting it as a potential therapeutic target for glaucoma.
Area of Science:
- Ophthalmology
- Cell Biology
- Molecular Biology
Background:
- Glaucoma involves fibrotic remodeling of the lamina cribrosa (LC), leading to optic nerve damage.
- Glaucomatous LC cells show increased extracellular matrix (ECM) production due to cellular stress.
- The role of CREB3L1, a transcription factor regulating ECM, in glaucomatous LC cells is unclear.
Purpose of the Study:
- To investigate the expression and function of CREB3L1 in human glaucomatous LC cells.
- To determine if CREB3L1 influences ECM production and cellular activity in glaucoma.
Main Methods:
- Primary human LC cells from glaucoma (GLC) and control (NLC) donors were used.
- CREB3L1 expression was measured via qRT-PCR and Western blot.
- siRNA was used to knock down CREB3L1 in GLC cells, followed by analysis of ECM gene transcription and cell metabolic activity.
Main Results:
- CREB3L1 mRNA and protein levels were significantly higher in GLC cells than NLC cells.
- CREB3L1 knockdown in GLC cells reduced ECM gene transcription (α-SMA, COL1A1, FN1).
- Suppression of CREB3L1 markedly decreased metabolic activity in glaucomatous LC cells.
Conclusions:
- CREB3L1 is identified as a key regulator of ECM gene expression and cellular behavior in glaucomatous LC cells.
- Elevated CREB3L1 may contribute to optic nerve head fibrotic remodeling in glaucoma.
- Targeting CREB3L1 pathways could be a potential therapeutic strategy for glaucoma.
