Editorial Type:
Ophthalmology

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

Caitlin A. Savagian Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53792-3220.

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Richard R. Dubielzig Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53792-3220.

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T. Michael Nork Department of Ophthalmology and Visual Sciences, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53792-3220.

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DOI:
https://doi.org/10.2460/ajvr.69.2.265
Volume/Issue:
Volume 69: Issue 2
Online Publication Date:
01 Feb 2008
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Abstract

Objective—To determine the effect of acute (clinical history of glaucoma for ≤ 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)-1α 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-1α in the retinas. Four of 5 specimens from eyes with chronic glaucoma had nuclear staining for HIF-1α in cells of the outer nuclear layer. Staining for HIF-1α 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.

Abstract

Objective—To determine the effect of acute (clinical history of glaucoma for ≤ 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)-1α 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-1α in the retinas. Four of 5 specimens from eyes with chronic glaucoma had nuclear staining for HIF-1α in cells of the outer nuclear layer. Staining for HIF-1α 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.

Contributor Notes

Supported by grants from the National Institutes of Health (T32 RR017503 [Savagian] and R01 EY014041 and P30 EY016665 [Nork]), American Health Assistance Foundation, Retina Research Foundation, Walter H. Helmerich Chair (Nork), and Research to Prevent Blindness.

The authors thank Janice M. Lokken, Kathleen S. Lieber, and Cassandra L. Miller and Drs. Charlene B. Y. Kim and Mitzi Zarfoss for technical assistance.

Address correspondence to Dr. Nork.
Cover American Journal of Veterinary Research
American Journal of Veterinary Research
Publication Date:
01 Feb 2008
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