Presentation Title (IN ALL CAPS)

DOWNREGULATION OF CYTOCHROME C OXIDASE FOLLOWING IOP ELEVATION IN RAT MODEL OF GLAUCOMA IS ATTENUATED BY αB-CRYSTALLIN CORE PEPTIDE (ABCP)

Departmental Affiliation and City, State, Zip for All Authors

Department of Chemistry and Biochemistry, Northridge, CA, 91330; North Texas Eye Research Institute, Fort Worth, TX 76107;North Texas Eye Research Institute, Fort Worth, TX 76107;North Texas Eye Research Institute, Fort Worth, TX 76107

Scientific Abstract

Glaucoma, a leading cause of blindness, is a neurodegenerative disease commonly associated with an elevated intraocular pressure (IOP) and damage to the optic nerve. Current treatments for glaucoma focus on lowering IOP through surgery or medication but some patients disease progresses even when IOP is managed at lower levels (Beidoe & Mousa, 2012). Research has shown that patients with Alzheimer’s disease, another neurodegenerative disease, have higher incidences of glaucoma than control groups (Tamura et al.,2005). IOP lowering should not be the only method of treatment and new treatments that promote neural protection and protect from loss of retinal ganglion cells (RGC) should be investigated.

Rats with elevated IOP were intraperitoneally injected with αB-crystallin core peptide (ABCP) which are chaperones from the heat shock protein family. After 5 weeks of IOP elevation rats were euthanized and optic nerves and retina sections were isolated. Axon counts were performed from paraphenylenediamine stained optic nerve sections. Retina sections were used for immunohistochemical analysis of the Cytochrome C Oxidase complex 6b2 subunit (Cox 6b2).

We believe that a downregulation of Cox 6b2, a necessary mitochondrial enzyme for maintenance of cellular respiration, contributes to neurodegeneration of RGC’s during glaucoma. Our previous data shown that intraperitoneally injected ABCP reduced the loss of RGC’s and neurodegeneration of the axons. We decided to analyze Cox 6b2 levels in IOP elevated rat retinas with and without ABCP treatment. We found that ABCP treatment sustained Cox 6b2 levels in IOP elevated retinas when compared to IOP-elevated and scrambled peptide treated rats.

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DOWNREGULATION OF CYTOCHROME C OXIDASE FOLLOWING IOP ELEVATION IN RAT MODEL OF GLAUCOMA IS ATTENUATED BY αB-CRYSTALLIN CORE PEPTIDE (ABCP)

Glaucoma, a leading cause of blindness, is a neurodegenerative disease commonly associated with an elevated intraocular pressure (IOP) and damage to the optic nerve. Current treatments for glaucoma focus on lowering IOP through surgery or medication but some patients disease progresses even when IOP is managed at lower levels (Beidoe & Mousa, 2012). Research has shown that patients with Alzheimer’s disease, another neurodegenerative disease, have higher incidences of glaucoma than control groups (Tamura et al.,2005). IOP lowering should not be the only method of treatment and new treatments that promote neural protection and protect from loss of retinal ganglion cells (RGC) should be investigated.

Rats with elevated IOP were intraperitoneally injected with αB-crystallin core peptide (ABCP) which are chaperones from the heat shock protein family. After 5 weeks of IOP elevation rats were euthanized and optic nerves and retina sections were isolated. Axon counts were performed from paraphenylenediamine stained optic nerve sections. Retina sections were used for immunohistochemical analysis of the Cytochrome C Oxidase complex 6b2 subunit (Cox 6b2).

We believe that a downregulation of Cox 6b2, a necessary mitochondrial enzyme for maintenance of cellular respiration, contributes to neurodegeneration of RGC’s during glaucoma. Our previous data shown that intraperitoneally injected ABCP reduced the loss of RGC’s and neurodegeneration of the axons. We decided to analyze Cox 6b2 levels in IOP elevated rat retinas with and without ABCP treatment. We found that ABCP treatment sustained Cox 6b2 levels in IOP elevated retinas when compared to IOP-elevated and scrambled peptide treated rats.

Manuscript Number

1008