Relative ability of aqueous humor from dogs with and without primary angle‐closure glaucoma andADAMTS10open‐angle glaucoma to catalyze or inhibit collagenolysis

Abstract

AbstractObjectiveThe objective of the study was to compare the ability of aqueous humor (AH) from dogs with primary angle‐closure glaucoma (CPACG), companion dogs without overt evidence of CPACG, and Beagles with and withoutADAMTS10open‐angle glaucoma (ADAMTS10‐OAG) to catalyze or inhibit collagenolysis.Animals studiedSeventeen normal pet dogs, 27 dogs with CPACG, 19 Beagles withADAMTS10‐OAG, and 4 unaffected Beagles.ProceduresA fluorescein‐based substrate degradation assay was used to assess AH proteolytic capacity. Samples were then assayed using the same substrate degradation assay, with recombinant activated matrix metalloproteinase‐2 (MMP‐2) added to measure protease inhibition effects.ResultsFor the protease activity assay, relative fluorescence (RF) for AH from normal pet dogs was 13.28 ± 2.25% of control collagenase while RF for AH from dogs with CPACG was 17.47 ± 4.67%; RF was 8.57 ± 1.72% forADAMTS10‐OAG Beagles and 7.99 ± 1.15% for unaffected Beagles. For the MMP‐2 inhibition assay, RF for AH from normal dogs was 34.96 ± 15.04% compared to MMP‐2 controls, while RF from dogs with CPACG was 16.69 ± 7.95%; RF was 85.85 ± 13.23% for Beagles withADAMTS10‐OAG and 94.51 ± 8.36% for unaffected Beagles. Significant differences were found between dogs with CPACG and both normal pet dogs and dogs withADAMTS10‐OAG and between normal pet dogs and both groups of Beagles.ConclusionsAH from dogs with CPACG is significantly more able to catalyze proteolysis and inhibit MMP‐2 than AH from normal dogs or dogs withADAMTS10‐OAG. Results suggest that pathogenesis may differ between CPACG andADAMTS10‐OAG.