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Editors Selection IGR 10-4

Basic research: Matrix GLA protein

Comment by Douglas Rhee on:

13384 Matrix GLA Protein Function in Human Trabecular Meshwork Cells: Inhibition of BMP2-Induced Calcification Process, Xue W; Wallin R; Olmsted-Davis EA et al., Investigative Ophthalmology and Visual Science, 2006; 47: 997-1007

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The underlying defect in the trabecular meshwork that causes the relatively elevated IOP in open-angle glaucoma is unknown. Previous work involving microarray studies looking at relative gene transcription levels identified matrix GLA protein (MGP) as one of the most highly expressed genes in human trabecular meshwork (TM). However, the function of MGP in TM is unknown.

In cartilage and arterial walls, MGP has been shown to inhibit calcification. To investigate MGP's role in human trabecular meshwork, Xue et al. (34) studied cell cultures of TM endothelial cells and perfused human anterior segments (i.e., Johnson model) for factors associated with bone formation (alkaline phosphatase activity, bone morphogenic protein-2 (BMP-2)) and measured calification (i.e., o-cresolphthalein) at the RNA and protein level. They also transfected TM cells with BMP-2 to show that these cells could calcify and that this calcification could be blocked by MGP. Their findings support the assertion that MGP is involved with inhibiting ossification/calcification of the TM. The authors propose that calcification may be a contributing pathophysiology to the increased outflow resistance of open-angle glaucoma.

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