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The dark phase intraocular pressure elevation and retinal ganglion cell degeneration in a rat model of experimental glaucoma.
Exp Eye Res. 2013 Jul; 112:21-8.EE

Abstract

Intraocular pressure (IOP) elevation is considered as a major risk factor causing the progression of vision deterioration in glaucoma. Although it is known that the IOP level changes widely throughout the day and night, how the dark or light phase IOP elevation contributes to retinal ganglion cell (RGC) degeneration is still largely unclear. To examine the profile of IOP, modified laser photocoagulation was applied to the trabecular meshwork of Brown Norway rats and both light and dark phase IOPs were monitored approximately 1-2 times a week. The relationship between IOP elevation and RGC degeneration was investigated while RGC body loss was analyzed with Rbpms immunolabeling on retinal wholemount and axonal injury in the optic nerve was semi-quantified. The baseline awake dark and light IOPs were 30.4 ± 2.7 and 20.2 ± 2.1 mmHg respectively. The average dark IOP was increased to 38.2 ± 3.2 mmHg for five weeks after the laser treatment on 270° trabecular meshwork. However, there was no significant loss of RGC body and axonal injury. After laser treatment on 330° trabecular meshwork, the dark and light IOPs were significantly increased to 43.8 ± 4.6 and 23 ± 3.7 mmHg respectively for 5 weeks. The cumulative dark and light IOP elevations were 277 ± 86 and 113 ± 50 mmHg days respectively while the cumulative total (light and dark) IOP elevation was 213 ± 114 mmHg days. After 5 weeks, regional RGC body loss of 29.5 ± 15.5% and moderate axonal injury were observed. Axonal injury and loss of RGC body had a high correlation with the cumulative total IOP elevation (R(2) = 0.60 and 0.65 respectively). There was an association between the cumulative dark IOP elevation and RGC body loss (R(2) = 0.37) and axonal injury (R(2) = 0.51) whereas the associations between neuronal damages and the cumulative light IOP elevation were weak (for RGC body loss, R(2) = 0.01; for axonal injury, R(2) = 0.26). Simple linear regression model analysis showed statistical significance for the relationships between the total cumulative IOP elevation and RGC body loss (P = 0.009), and axonal injury (P = 0.016). To examine the role of light and dark IOP elevation in RGC body loss and axonal injury, analyses for the association between different light/dark IOP factors and percentage of RGC body loss/axonal injury grading were performed and only the association between the cumulative dark IOP elevation and axonal injury showed statistical significance (P = 0.033). The findings demonstrated that the cumulative total (light and dark) IOP elevation is a risk factor to RGC degeneration in a rat model of experimental glaucoma using modified partial laser photocoagulation at 330° trabecular meshwork. Further investigations are required to understand the role of longer term light and dark phase IOP elevation contributing to the progression of degeneration in different compartments of RGCs.

Authors+Show Affiliations

Jules Stein Eye Institute, David Geffen School of Medicine, University of California Los Angeles, 100 Stein Plaza, Los Angeles, CA 90095, United States. kwong@jsei.ucla.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

23603611

Citation

Kwong, Jacky M K., et al. "The Dark Phase Intraocular Pressure Elevation and Retinal Ganglion Cell Degeneration in a Rat Model of Experimental Glaucoma." Experimental Eye Research, vol. 112, 2013, pp. 21-8.
Kwong JM, Vo N, Quan A, et al. The dark phase intraocular pressure elevation and retinal ganglion cell degeneration in a rat model of experimental glaucoma. Exp Eye Res. 2013;112:21-8.
Kwong, J. M., Vo, N., Quan, A., Nam, M., Kyung, H., Yu, F., Piri, N., & Caprioli, J. (2013). The dark phase intraocular pressure elevation and retinal ganglion cell degeneration in a rat model of experimental glaucoma. Experimental Eye Research, 112, 21-8. https://doi.org/10.1016/j.exer.2013.04.008
Kwong JM, et al. The Dark Phase Intraocular Pressure Elevation and Retinal Ganglion Cell Degeneration in a Rat Model of Experimental Glaucoma. Exp Eye Res. 2013;112:21-8. PubMed PMID: 23603611.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The dark phase intraocular pressure elevation and retinal ganglion cell degeneration in a rat model of experimental glaucoma. AU - Kwong,Jacky M K, AU - Vo,Nancy, AU - Quan,Ann, AU - Nam,Michael, AU - Kyung,Haksu, AU - Yu,Fei, AU - Piri,Natik, AU - Caprioli,Joseph, Y1 - 2013/04/18/ PY - 2013/02/05/received PY - 2013/03/28/revised PY - 2013/04/10/accepted PY - 2013/4/23/entrez PY - 2013/4/23/pubmed PY - 2013/9/21/medline SP - 21 EP - 8 JF - Experimental eye research JO - Exp Eye Res VL - 112 N2 - Intraocular pressure (IOP) elevation is considered as a major risk factor causing the progression of vision deterioration in glaucoma. Although it is known that the IOP level changes widely throughout the day and night, how the dark or light phase IOP elevation contributes to retinal ganglion cell (RGC) degeneration is still largely unclear. To examine the profile of IOP, modified laser photocoagulation was applied to the trabecular meshwork of Brown Norway rats and both light and dark phase IOPs were monitored approximately 1-2 times a week. The relationship between IOP elevation and RGC degeneration was investigated while RGC body loss was analyzed with Rbpms immunolabeling on retinal wholemount and axonal injury in the optic nerve was semi-quantified. The baseline awake dark and light IOPs were 30.4 ± 2.7 and 20.2 ± 2.1 mmHg respectively. The average dark IOP was increased to 38.2 ± 3.2 mmHg for five weeks after the laser treatment on 270° trabecular meshwork. However, there was no significant loss of RGC body and axonal injury. After laser treatment on 330° trabecular meshwork, the dark and light IOPs were significantly increased to 43.8 ± 4.6 and 23 ± 3.7 mmHg respectively for 5 weeks. The cumulative dark and light IOP elevations were 277 ± 86 and 113 ± 50 mmHg days respectively while the cumulative total (light and dark) IOP elevation was 213 ± 114 mmHg days. After 5 weeks, regional RGC body loss of 29.5 ± 15.5% and moderate axonal injury were observed. Axonal injury and loss of RGC body had a high correlation with the cumulative total IOP elevation (R(2) = 0.60 and 0.65 respectively). There was an association between the cumulative dark IOP elevation and RGC body loss (R(2) = 0.37) and axonal injury (R(2) = 0.51) whereas the associations between neuronal damages and the cumulative light IOP elevation were weak (for RGC body loss, R(2) = 0.01; for axonal injury, R(2) = 0.26). Simple linear regression model analysis showed statistical significance for the relationships between the total cumulative IOP elevation and RGC body loss (P = 0.009), and axonal injury (P = 0.016). To examine the role of light and dark IOP elevation in RGC body loss and axonal injury, analyses for the association between different light/dark IOP factors and percentage of RGC body loss/axonal injury grading were performed and only the association between the cumulative dark IOP elevation and axonal injury showed statistical significance (P = 0.033). The findings demonstrated that the cumulative total (light and dark) IOP elevation is a risk factor to RGC degeneration in a rat model of experimental glaucoma using modified partial laser photocoagulation at 330° trabecular meshwork. Further investigations are required to understand the role of longer term light and dark phase IOP elevation contributing to the progression of degeneration in different compartments of RGCs. SN - 1096-0007 UR - https://www.unboundmedicine.com/medline/citation/23603611/The_dark_phase_intraocular_pressure_elevation_and_retinal_ganglion_cell_degeneration_in_a_rat_model_of_experimental_glaucoma_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4835(13)00096-1 DB - PRIME DP - Unbound Medicine ER -