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Degenerative effects in rat eyes after experimental ocular hypertension
This study was used to evaluate the degenerative effects on the retina and eye-cup sections after experimental induction of acute ocular hypertension on animal models. In particular, vascular events were directly focused in this research in order to assess the vascular remodeling after transient ocu...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
PAGEPress Publications
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567761/ https://www.ncbi.nlm.nih.gov/pubmed/23361238 http://dx.doi.org/10.4081/ejh.2012.e42 |
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author | Scarsella, G. Nebbioso, M. Stefanini, S. Librando, A. Pescosolido, N. |
author_facet | Scarsella, G. Nebbioso, M. Stefanini, S. Librando, A. Pescosolido, N. |
author_sort | Scarsella, G. |
collection | PubMed |
description | This study was used to evaluate the degenerative effects on the retina and eye-cup sections after experimental induction of acute ocular hypertension on animal models. In particular, vascular events were directly focused in this research in order to assess the vascular remodeling after transient ocular hypertension on rat models. After local anaesthesia by administration of eye drops of 0.4% oxibuprocaine, 16 male adult Wistar rats were injected in the anterior chamber of the right eye with 15 µL of methylcellulose (MTC) 2% in physiological solution. The morphology and the vessels of the retina and eye-cup sections were examined in animals sacrificed 72 h after induction of ocular hypertension. In retinal fluorescein angiographies (FAGs), by means of fluorescein isothiocyanate-coniugated dextran (FITC), the radial venules showed enlargements and increased branching, while the arterioles appeared focally thickened. The length and size of actually perfused vessels appeared increased in the whole superficial plexus. In eye-cup sections of MTC-injected animals, in deep plexus and connecting layer there was a bigger increase of vessels than in controls. Moreover, the immunolocalization of astrocytic marker glial fibrillary acidic protein (GFAP) revealed its increased expression in internal limiting membrane and ganglion cell layer, as well as its presence in Müller cells. Finally, the pro-angiogenic factor vascular endothelial growth factor (VEGF) was found to be especially expressed by neurones of ganglion cell layer, both in control and in MTC-injected eyes. The data obtained in this experimental model on the interactions among glia, vessels and neurons should be useful to evaluate if also in glaucomatous patients the activation of vessel-adjacent glial cells might play key roles in following neuronal dysfunction. |
format | Online Article Text |
id | pubmed-3567761 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | PAGEPress Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-35677612013-02-11 Degenerative effects in rat eyes after experimental ocular hypertension Scarsella, G. Nebbioso, M. Stefanini, S. Librando, A. Pescosolido, N. Eur J Histochem Original Paper This study was used to evaluate the degenerative effects on the retina and eye-cup sections after experimental induction of acute ocular hypertension on animal models. In particular, vascular events were directly focused in this research in order to assess the vascular remodeling after transient ocular hypertension on rat models. After local anaesthesia by administration of eye drops of 0.4% oxibuprocaine, 16 male adult Wistar rats were injected in the anterior chamber of the right eye with 15 µL of methylcellulose (MTC) 2% in physiological solution. The morphology and the vessels of the retina and eye-cup sections were examined in animals sacrificed 72 h after induction of ocular hypertension. In retinal fluorescein angiographies (FAGs), by means of fluorescein isothiocyanate-coniugated dextran (FITC), the radial venules showed enlargements and increased branching, while the arterioles appeared focally thickened. The length and size of actually perfused vessels appeared increased in the whole superficial plexus. In eye-cup sections of MTC-injected animals, in deep plexus and connecting layer there was a bigger increase of vessels than in controls. Moreover, the immunolocalization of astrocytic marker glial fibrillary acidic protein (GFAP) revealed its increased expression in internal limiting membrane and ganglion cell layer, as well as its presence in Müller cells. Finally, the pro-angiogenic factor vascular endothelial growth factor (VEGF) was found to be especially expressed by neurones of ganglion cell layer, both in control and in MTC-injected eyes. The data obtained in this experimental model on the interactions among glia, vessels and neurons should be useful to evaluate if also in glaucomatous patients the activation of vessel-adjacent glial cells might play key roles in following neuronal dysfunction. PAGEPress Publications 2012-10-08 /pmc/articles/PMC3567761/ /pubmed/23361238 http://dx.doi.org/10.4081/ejh.2012.e42 Text en ©Copyright G. Scarsella et al., 2012 This work is licensed under a Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Licensee PAGEPress, Italy |
spellingShingle | Original Paper Scarsella, G. Nebbioso, M. Stefanini, S. Librando, A. Pescosolido, N. Degenerative effects in rat eyes after experimental ocular hypertension |
title | Degenerative effects in rat eyes after experimental ocular hypertension |
title_full | Degenerative effects in rat eyes after experimental ocular hypertension |
title_fullStr | Degenerative effects in rat eyes after experimental ocular hypertension |
title_full_unstemmed | Degenerative effects in rat eyes after experimental ocular hypertension |
title_short | Degenerative effects in rat eyes after experimental ocular hypertension |
title_sort | degenerative effects in rat eyes after experimental ocular hypertension |
topic | Original Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567761/ https://www.ncbi.nlm.nih.gov/pubmed/23361238 http://dx.doi.org/10.4081/ejh.2012.e42 |
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