Comparison of the distribution of glial fibrillary acidic protein, heat shock protein 60, and hypoxia-inducible factor-1alpha in retinas from glaucomatous and normal canine eyes.

Michael Nork // Publications // Richard Dubielzig // Feb 01 2008

PubMed ID: 18241025

Author(s): Savagian CA, Dubielzig RR, Nork TM. Comparison of the distribution of glial fibrillary acidic protein, heat shock protein 60, and hypoxia-inducible factor-1alpha in retinas from glaucomatous and normal canine eyes. Am J Vet Res. 2008 Feb;69(2):265-72. doi: 10.2460/ajvr.69.2.265. PMID 18241025

Journal: American Journal Of Veterinary Research, Volume 69, Issue 2, Feb 2008

OBJECTIVE To determine the effect of acute (clinical history of glaucoma for <or= 2 days) and chronic (clinical history of glaucoma for 7 days) goniodysgenesis-related glaucoma on various stress-inducible proteins in canine retinas.

SAMPLE POPULATION 15 canine retinas (5 from control eyes, 5 from eyes with acute glaucoma, and 5 from eyes with chronic glaucoma).

PROCEDURES Globes were obtained from the Comparative Ocular Pathology Laboratory of Wisconsin. Eyes were characterized on the basis of clinical history. The distribution of glial fibrillary acidic protein (GFAP), heat shock protein (HSP) 60, and hypoxia-inducible factor (HIF)-1alpha was determined by use of immunohistochemical analysis.

RESULTS Intensity of GFAP staining increased with temporal progression of glaucoma. In specimens from eyes with acute glaucoma, staining for HSP 60 was more variable among eyes, compared with that of the control eyes, whereas specimens from eyes with chronic glaucoma typically had less HSP 60 staining than was evident in the control eyes. Neither the control eyes nor specimens from the eyes with acute glaucoma had nuclear staining for HIF-1alpha in the retinas. Four of 5 specimens from eyes with chronic glaucoma had nuclear staining for HIF-1alpha in cells of the outer nuclear layer. Staining for HIF-1alpha was distributed segmentally in regions of more severe atrophy and disorganization.

CONCLUSIONS AND CLINICAL RELEVANCE Results of the study reported here supported a clinically evident, rapidly progressive disease with a shift in cell regulation between acute and chronic glaucoma and also supported ischemia as a mechanism of retinal injury in this disease.