<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pumphrey SA</submitter><funding>NEI NIH HHS</funding><funding>BrightFocus Foundation</funding><funding>National Institutes of Health</funding><funding>NIH HHS</funding><pagination>238-247</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10904665</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>27(3)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>The 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 without ADAMTS10 open-angle glaucoma (ADAMTS10-OAG) to catalyze or inhibit collagenolysis.&lt;h4>Animals studied&lt;/h4>Seventeen normal pet dogs, 27 dogs with CPACG, 19 Beagles with ADAMTS10-OAG, and 4 unaffected Beagles.&lt;h4>Procedures&lt;/h4>A 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.&lt;h4>Results&lt;/h4>For 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% for ADAMTS10-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 with ADAMTS10-OAG and 94.51 ± 8.36% for unaffected Beagles. Significant differences were found between dogs with CPACG and both normal pet dogs and dogs with ADAMTS10-OAG and between normal pet dogs and both groups of Beagles.&lt;h4>Conclusions&lt;/h4>AH from dogs with CPACG is significantly more able to catalyze proteolysis and inhibit MMP-2 than AH from normal dogs or dogs with ADAMTS10-OAG. Results suggest that pathogenesis may differ between CPACG and ADAMTS10-OAG.</pubmed_abstract><journal>Veterinary ophthalmology</journal><pubmed_title>Relative ability of aqueous humor from dogs with and without primary angle-closure glaucoma and ADAMTS10 open-angle glaucoma to catalyze or inhibit collagenolysis.</pubmed_title><pmcid>PMC10904665</pmcid><funding_grant_id>R01 EY025752</funding_grant_id><funding_grant_id>R01-EY025752</funding_grant_id><funding_grant_id>R01 EY032478</funding_grant_id><funding_grant_id>G2022007S</funding_grant_id><funding_grant_id>R01-EY032478</funding_grant_id><funding_grant_id>R01‐EY025752</funding_grant_id><funding_grant_id>R01‐EY032478</funding_grant_id><pubmed_authors>Harman CD</pubmed_authors><pubmed_authors>Sweigart B</pubmed_authors><pubmed_authors>Anderson AL</pubmed_authors><pubmed_authors>Pumphrey SA</pubmed_authors><pubmed_authors>Komaromy AM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Relative ability of aqueous humor from dogs with and without primary angle-closure glaucoma and ADAMTS10 open-angle glaucoma to catalyze or inhibit collagenolysis.</name><description>&lt;h4>Objective&lt;/h4>The 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 without ADAMTS10 open-angle glaucoma (ADAMTS10-OAG) to catalyze or inhibit collagenolysis.&lt;h4>Animals studied&lt;/h4>Seventeen normal pet dogs, 27 dogs with CPACG, 19 Beagles with ADAMTS10-OAG, and 4 unaffected Beagles.&lt;h4>Procedures&lt;/h4>A 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.&lt;h4>Results&lt;/h4>For 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% for ADAMTS10-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 with ADAMTS10-OAG and 94.51 ± 8.36% for unaffected Beagles. Significant differences were found between dogs with CPACG and both normal pet dogs and dogs with ADAMTS10-OAG and between normal pet dogs and both groups of Beagles.&lt;h4>Conclusions&lt;/h4>AH from dogs with CPACG is significantly more able to catalyze proteolysis and inhibit MMP-2 than AH from normal dogs or dogs with ADAMTS10-OAG. Results suggest that pathogenesis may differ between CPACG and ADAMTS10-OAG.</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 May</publication><modification>2025-07-12T03:04:34.465Z</modification><creation>2025-07-12T03:04:34.465Z</creation></dates><accession>S-EPMC10904665</accession><cross_references><pubmed>37658474</pubmed><doi>10.1111/vop.13143</doi></cross_references></HashMap>