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Updated: Jan 28, 2026
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Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
Published on: June 20, 2015
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Mechanical stretch upregulates connexin43 in human trabecular meshwork cells
Nikoleta Tellios1, Mary Feng2, Nancy Chen3
1School of Medicine, University College Cork, Cork, Ireland.
Clinical & Experimental Ophthalmology
|March 1, 2019
Summary
Mechanical stretch increases connexin43 (Cx43) expression and intercellular communication in human trabecular meshwork cells, potentially contributing to primary open angle glaucoma (POAG) pathogenesis.
Area of Science:
- Ophthalmology
- Cell Biology
- Biochemistry
Background:
- Primary open angle glaucoma (POAG) is characterized by elevated intraocular pressure (IOP) and trabecular meshwork (TM) dysfunction.
- Connexin43 (Cx43), encoded by the GJA1 gene, is a crucial gap junction protein in the TM, facilitating intercellular communication.
Purpose of the Study:
- To investigate the impact of mechanical stretch on cultured human trabecular meshwork cells (hTMCs).
- To determine the effect of mechanical stretch on Cx43 expression and function within hTMCs.
Main Methods:
- hTMCs were subjected to cyclic mechanical stretch (15% strain, 1 Hz) for 48 hours.
- Apoptosis and necrosis were assessed using colorimetric assays.
- Cx43 and GJA1 expression were analyzed via RT-PCR, immunoblotting, and immunofluorescence; intercellular communication was measured by Lucifer Yellow dye migration.
Main Results:
- Mechanical stretch significantly elevated apoptosis and necrosis rates in hTMCs.
- Stretch induced a significant upregulation of GJA1 mRNA and Cx43 protein expression.
- Increased Cx43 protein levels correlated with enhanced intercellular communication.
Conclusions:
- Mechanical stretch increases GJA1 gene and Cx43 protein expression, alongside heightened intercellular communication in hTMCs.
- Stretch is injurious to hTMCs, and the observed Cx43 upregulation is a novel finding.
- This study provides insights into TM injury mechanisms relevant to POAG.
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