The Schlager mouse as a model of altered retinal phenotype

Hypertension is a risk factor for a large number of vision-threatening eye disorders. In this study, we investigated for the first time the retinal neural structure of the hypertensive BPH/2J mouse (Schlager mouse) and compared it to its control counterpart, the normotensive BPN/3J strain. The BPH/2...

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Main Authors: Lakshini Y Herat, Aaron L Magno, Márcio G Kiuchi, Kristy L Jackson, Revathy Carnagarin, Geoffrey A Head, Markus P Schlaich, Vance B Matthews
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2020-01-01
Series:Neural Regeneration Research
Subjects:
Online Access:http://www.nrronline.org/article.asp?issn=1673-5374;year=2020;volume=15;issue=3;spage=512;epage=518;aulast=Herat
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author Lakshini Y Herat
Aaron L Magno
Márcio G Kiuchi
Kristy L Jackson
Revathy Carnagarin
Geoffrey A Head
Markus P Schlaich
Vance B Matthews
author_facet Lakshini Y Herat
Aaron L Magno
Márcio G Kiuchi
Kristy L Jackson
Revathy Carnagarin
Geoffrey A Head
Markus P Schlaich
Vance B Matthews
author_sort Lakshini Y Herat
collection DOAJ
description Hypertension is a risk factor for a large number of vision-threatening eye disorders. In this study, we investigated for the first time the retinal neural structure of the hypertensive BPH/2J mouse (Schlager mouse) and compared it to its control counterpart, the normotensive BPN/3J strain. The BPH/2J mouse is a selectively inbred mouse strain that develops chronic hypertension due to elevated sympathetic nervous system activity. When compared to the BPN/3J strain, the hypertensive BPH/2J mice showed a complete loss of outer layers of the neural retina at 21 weeks of age, which was indicative of a severe vision-threatening disease potentially caused by hypertension. To elucidate whether the retinal neural phenotype in the BPH/2J strain was attributed to increased BP, we investigated the neural retina of both BPN/3J and BPH/2J mice at 4 weeks of age. Our preliminary results showed for the first time that the BPH/2J strain develops severe retinal neural damage at a young age. Our findings suggest that the retinal phenotype in the BPH/2J mouse is possibly due to elevated blood pressure and may be contributed by an early onset spontaneous mutation which is yet to be identified or a congenital defect occurring in this strain. Further characterization of the BPH/2J mouse strain is likely to i) elucidate gene defects underlying retinal disease; ii) understand mechanisms leading to neural retinal disease and iii) permit testing of molecules for translational research to interfere with the progression of retinal disease. The animal experiments were performed with the approval of the Royal Perth Hospital Animal Ethics Committee (R535/17-18) on June 1, 2017.
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spelling doaj.art-8eabb1e6977845848870dfdc7afcb5e02022-12-22T02:27:45ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53742020-01-0115351251810.4103/1673-5374.266069The Schlager mouse as a model of altered retinal phenotypeLakshini Y HeratAaron L MagnoMárcio G KiuchiKristy L JacksonRevathy CarnagarinGeoffrey A HeadMarkus P SchlaichVance B MatthewsHypertension is a risk factor for a large number of vision-threatening eye disorders. In this study, we investigated for the first time the retinal neural structure of the hypertensive BPH/2J mouse (Schlager mouse) and compared it to its control counterpart, the normotensive BPN/3J strain. The BPH/2J mouse is a selectively inbred mouse strain that develops chronic hypertension due to elevated sympathetic nervous system activity. When compared to the BPN/3J strain, the hypertensive BPH/2J mice showed a complete loss of outer layers of the neural retina at 21 weeks of age, which was indicative of a severe vision-threatening disease potentially caused by hypertension. To elucidate whether the retinal neural phenotype in the BPH/2J strain was attributed to increased BP, we investigated the neural retina of both BPN/3J and BPH/2J mice at 4 weeks of age. Our preliminary results showed for the first time that the BPH/2J strain develops severe retinal neural damage at a young age. Our findings suggest that the retinal phenotype in the BPH/2J mouse is possibly due to elevated blood pressure and may be contributed by an early onset spontaneous mutation which is yet to be identified or a congenital defect occurring in this strain. Further characterization of the BPH/2J mouse strain is likely to i) elucidate gene defects underlying retinal disease; ii) understand mechanisms leading to neural retinal disease and iii) permit testing of molecules for translational research to interfere with the progression of retinal disease. The animal experiments were performed with the approval of the Royal Perth Hospital Animal Ethics Committee (R535/17-18) on June 1, 2017.http://www.nrronline.org/article.asp?issn=1673-5374;year=2020;volume=15;issue=3;spage=512;epage=518;aulast=Heratblood pressure; eye; hypertension; mice; neural regeneration; retina; Schlager mouse; sympathetic nervous system
spellingShingle Lakshini Y Herat
Aaron L Magno
Márcio G Kiuchi
Kristy L Jackson
Revathy Carnagarin
Geoffrey A Head
Markus P Schlaich
Vance B Matthews
The Schlager mouse as a model of altered retinal phenotype
Neural Regeneration Research
blood pressure; eye; hypertension; mice; neural regeneration; retina; Schlager mouse; sympathetic nervous system
title The Schlager mouse as a model of altered retinal phenotype
title_full The Schlager mouse as a model of altered retinal phenotype
title_fullStr The Schlager mouse as a model of altered retinal phenotype
title_full_unstemmed The Schlager mouse as a model of altered retinal phenotype
title_short The Schlager mouse as a model of altered retinal phenotype
title_sort schlager mouse as a model of altered retinal phenotype
topic blood pressure; eye; hypertension; mice; neural regeneration; retina; Schlager mouse; sympathetic nervous system
url http://www.nrronline.org/article.asp?issn=1673-5374;year=2020;volume=15;issue=3;spage=512;epage=518;aulast=Herat
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