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Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis
Published on: June 3, 2018
Effect of CD44 suppression by antisense oligonucleotide on attachment of human trabecular meshwork cells to HA
1Department of Ophthalmology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Insights
Suppressing CD44 in human trabecular meshwork cells reduced their attachment to hyaluronic acid. This suggests CD44 may influence primary open-angle glaucoma (POAG) development by altering cell adhesion.
Area of Science:
- Ocular biology
- Cellular adhesion mechanisms
- Glaucoma pathogenesis
Background:
- CD44 is a cell surface receptor involved in cell adhesion and extracellular matrix interactions.
- Hyaluronic acid (HA) is a major component of the extracellular matrix in the trabecular meshwork.
- Primary open-angle glaucoma (POAG) is a leading cause of irreversible blindness, characterized by progressive optic nerve damage.
Purpose of the Study:
- To investigate the role of CD44 in the attachment of human trabecular meshwork (HTM) cells to hyaluronic acid (HA).
- To explore the potential involvement of CD44 in the pathogenesis of primary open-angle glaucoma (POAG).
Main Methods:
- HTM cells were treated with a CD44-specific antisense oligonucleotide to suppress CD44 expression.
- CD44 suppression was confirmed using RT-PCR and Western blotting.
- Cell attachment to HA was quantified using the MTT assay.
Main Results:
- CD44-specific antisense oligonucleotide effectively suppressed CD44 expression in HTM cells.
- Suppression of CD44 led to a concentration-dependent decrease in HTM cell adhesion to HA.
- This indicates a significant role for CD44 in mediating HTM cell attachment to HA.
Conclusions:
- CD44 plays a crucial role in the adhesion of human trabecular meshwork cells to hyaluronic acid.
- CD44-mediated cell adhesion may be a contributing factor in the pathogenesis of primary open-angle glaucoma (POAG).
- Targeting CD44 could represent a potential therapeutic strategy for POAG.
Abstract:
The effects of suppression of CD44 by CD44-specific antisense oligonucleotide on attachment of human trabecular meshwork cells to hyaluronic acid (HA) were observed and the possible relationship between CD44 and primary open-angle glaucoma (POAG) investigated. CD44-specific antisense oligonucleotide was delivered with cationic lipid to cultured human trabecular meshwork cells. The expression of CD44 suppressed by CD44-specific antisense oligonucleotide was detected by RT-PCR and Western blotting. The effect of CD44 suppression by specific antisense oligonucleotide on attachment of trabecular meshwork cells to HA was measured by MTT assay. Results showed that expression of CD44 was suppressed by CD44-specific antisense oligonucleotide. Antisense oligonucleotide also suppressed the adhesion of human trabecular meshwork cells to HA in a concentration dependent manner. It was concluded that attachment of human trabecular meshwork cells to HA was decreased when CD44 was suppressed by specific antisense oligonucleotide. CD44 might play a role in pathogenesis of POAG by affecting the adhesion of trabecular meshwork cells to HA.
