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Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye

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Published on: June 20, 2015

Evidence for a calcification process in the trabecular meshwork.

Teresa Borrás¹, Núria Comes

¹Department of Ophthalmology, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7041, USA. tborras@med.unc.edu

Experimental Eye Research

|December 17, 2008

Summary

The human trabecular meshwork (TM) may undergo calcification, similar to bone. Key genes regulating mineralization, like Matrix Gla (MGP), are highly expressed in the TM, suggesting a role in this process.

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Area of Science:

Ocular Biology
Biochemistry
Calcification Pathways

Background:

The human trabecular meshwork (TM) expresses genes linked to physiological and pathological calcification.
Matrix Gla (MGP) protein, a vitamin K-dependent inhibitor of calcification, is highly expressed in the TM.
TM cells possess active gamma-carboxylase, essential for MGP activation.

Purpose of the Study:

To review evidence supporting a mineralization process within the TM.
To analyze the expression of twenty regulatory calcification genes in the TM.
To compare TM gene expression patterns with known calcification literature.

Main Methods:

Literature review of twenty regulatory calcification genes.
Analysis of gene expression in TM using heat maps from microarrays.
Examination of MGP's role in regulating alkaline phosphatase (ALP) activity.

Main Results:

TM highly expresses MGP, a potent inhibitor of calcification.
Silencing MGP increases ALP activity, a marker of calcification.
Overexpressing MGP reduces BMP2-induced ALP activity.
TM gene expression shows similarities to calcification processes in other tissues.

Conclusions:

Evidence suggests a potential mineralization process in the TM.
Mechanical stress in the TM may influence calcification.
Further research on calcification genes and knockout models is needed to confirm TM's role in calcification.