| Item type: | Article | ||||
|---|---|---|---|---|---|
| Journal or Publication Title: | Journal of Cellular and Molecular Medicine | ||||
| Publisher: | Wiley | ||||
| Place of Publication: | HOBOKEN | ||||
| Volume: | 23 | ||||
| Number of Issue or Book Chapter: | 8 | ||||
| Page Range: | pp. 5497-5507 | ||||
| Date: | 2019 | ||||
| Institutions: | Biology, Preclinical Medicine > Institut für Anatomie Biology, Preclinical Medicine > Institut für Anatomie > Lehrstuhl für Humananatomie und Embryologie Biology, Preclinical Medicine > Institut für Anatomie > Lehrstuhl für Humananatomie und Embryologie > Prof. Dr. Ernst Tamm | ||||
| Identification Number: |
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| Keywords: | INDUCED OCULAR HYPERTENSION; OPTIC-NERVE HEAD; INTRAOCULAR-PRESSURE; RISK-FACTORS; DBA/2J MICE; MULLER GLIA; PREVALENCE; ASTROCYTES; DAMAGE; INNER; electroretinogram; primary open-angle glaucoma; retinal ganglion cells; ss B1-CTGF | ||||
| Dewey Decimal Classification: | 500 Science > 570 Life sciences | ||||
| Status: | Published | ||||
| Refereed: | Yes, this version has been refereed | ||||
| Created at the University of Regensburg: | Yes | ||||
| Item ID: | 48390 |
Web of ScienceAbstract
Primary open-angle glaucoma (POAG) is one of the most common causes for blindness worldwide. Although an elevated intraocular pressure (IOP) is the main risk factor, the exact pathology remained indistinguishable. Therefore, it is necessary to have appropriate models to investigate these mechanisms. Here, we analysed a transgenic glaucoma mouse model (ss B1-CTGF) to elucidate new possible ...
Abstract
Primary open-angle glaucoma (POAG) is one of the most common causes for blindness worldwide. Although an elevated intraocular pressure (IOP) is the main risk factor, the exact pathology remained indistinguishable. Therefore, it is necessary to have appropriate models to investigate these mechanisms. Here, we analysed a transgenic glaucoma mouse model (ss B1-CTGF) to elucidate new possible mechanisms of the disease. Therefore, IOP was measured in ss B1-CTGF and wildtype mice at 5, 10 and 15 weeks of age. At 5 and 10 weeks, the IOP in both groups were comparable (P > 0.05). After 15 weeks, a significant elevated IOP was measured in ss B1-CTGF mice (P < 0.001). At 15 weeks, electroretinogram measurements were performed and both the a- and b-wave amplitudes were significantly decreased in ss B1-CTGF retinae (both P < 0.01). Significantly fewer Brn-3a(+) retinal ganglion cells (RGCs) were observed in the ss B1-CTGF group on flatmounts (P = 0.02), cross-sections (P < 0.001) and also via quantitative real-time PCR (P = 0.02). Additionally, significantly more cleaved caspase 3(+) RGCs were seen in the ss B1-CTGF group (P = 0.002). Furthermore, a decrease in recoverin(+) cells was observable in the ss B1-CTGF animals (P = 0.004). Accordingly, a significant down-regulation of Recoverin mRNA levels were noted (P < 0.001). Gfap expression, on the other hand, was higher in ss B1-CTGF retinae (P = 0.023). Additionally, more glutamine synthetase signal was noted (P = 0.04). Although no alterations were observed regarding photoreceptors via immunohistology, a significant decrease of Rhodopsin (P = 0.003) and Opsin mRNA (P = 0.03) was noted. We therefore assume that the ss B1-CTGF mouse could serve as an excellent model for better understanding the pathomechanisms in POAG.
Metadata last modified: 03 Sep 2021 09:55
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