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Glaucomatous trabecular meshworks show increased markers of calcification
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Samples of human trabecular meshwork obtained from deceased glaucoma patients showed significantly increased levels of alkaline phosphatase enzyme activity, a marker of calcification, a laboratory study found.
Terete Borrás, PhD, and colleagues at the University of North Carolina School of Medicine, Chapel Hill, compared levels of calcification markers in trabecular meshwork samples from glaucomatous and normal eyes. They found alkaline phosphatase enzyme activity levels averaged 7.3 ng per µg of DNA for control specimens compared with 37 ng per µg of DNA in glaucomatous tissue samples, according to the study.
Investigators also found that dexamethasone and transforming growth factor beta 2 (TGF?2), which are factors associated with glaucoma, caused a significant up-regulation of alkaline phosphatase activity in two primary cell lines. In addition, glaucomatous tissue showed a –4.4-fold reduction in the expression of the gene that encodes matrix Gla, which inhibits calcification, according to the study.
"The increased activity of the calcification marker, [alkaline phosphatase], in glaucomatous trabecular meshworks might be indicative of an undergoing mineralization process during development of the disease," the authors said. "Inhibition of the calcification mechanism represented by the presence of active [matrix Gla] appears to be compromised in glaucomatous tissue."
The study is published in the July issue of Investigative Ophthalmology & Visual Science.