The Experts below are selected from a list of 240 Experts worldwide ranked by ideXlab platform
Akira Hara - One of the best experts on this subject based on the ideXlab platform.
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Retinal Cell Degeneration in Animal Models
International journal of molecular sciences, 2016Co-Authors: Masayuki Niwa, Hitomi Aoki, Akihiro Hirata, Hiroyuki Tomita, Paul G. Green, Akira HaraAbstract:The aim of this review is to provide an overview of various retinal Cell Degeneration models in animal induced by chemicals (N-methyl-d-aspartate- and CoCl2-induced), autoimmune (experimental autoimmune encephalomyelitis), mechanical stress (optic nerve crush-induced, light-induced) and ischemia (transient retinal ischemia-induced). The target regions, pathology and proposed mechanism of each model are described in a comparative fashion. Animal models of retinal Cell Degeneration provide insight into the underlying mechanisms of the disease, and will facilitate the development of novel effective therapeutic drugs to treat retinal Cell damage.
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Localization of septin 8 in murine retina, and spatiotemporal expression of septin 8 in a murine model of photoreceptor Cell Degeneration.
Neuroscience letters, 2007Co-Authors: Akira Hara, Masayuki Niwa, Hitomi Aoki, Takahiro Kunisada, Ayako Taguchi, Yasuhiro Yamada, Hidenori Ito, Koh-ichi Nagata, Hideki MoriAbstract:The septins, which form a conserved family of cytoskeletal GTP-binding proteins in mammals, comprise stable heteromeric complexes and have diverse roles in protein scaffolding, cytokinesis, vesicle trafficking and plasma membrane integrity following Cell division. The goal of this study was to determine the localization of septin 8 in murine adult retina, and analyze the spatiotemporal expression of septin 8 in a murine model of photoreceptor Cell Degeneration. Expression of septin 8 in the normal retina of mouse and rat was observed by using immunohistochemistry and Western blotting. Furthermore, time course of the expression of septin 8 in mouse photoreceptor Cell Degeneration were examined by immunohistochemistry combined with hematoxylin and eosin staining, and in situ DNA fragment labeling method. In normal mouse and rat retina, localization of septin 8 is restricted in nuclei of photoreceptor Cells. 96 h after intravitreal injection of cobalt chloride most photoreceptor Cells lost septin 8 immunostaining at the same time as nuclear DNA fragmentation. The results of this study show that septin 8 protein is present in the specific location within the retina. Furthermore, the disappearance of septin 8 in the nuclei of photoreceptor Cells is concomitant with nuclear DNA fragmentation. This suggests that loss of septin 8 could be a useful prognostic indicator for photoreceptor Cell Degeneration.
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A new model of retinal photoreceptor Cell Degeneration induced by a chemical hypoxia-mimicking agent, cobalt chloride.
Brain research, 2006Co-Authors: Akira Hara, Masayuki Niwa, Hitomi Aoki, Masako Kumada, Takahiro Kunisada, Takeru Oyama, Tetsuya Yamamoto, Osamu Kozawa, Hideki MoriAbstract:Retinal photoreceptor Cell Degeneration was induced by cobalt chloride, a chemical hypoxia-mimicking agent in rodents. Time course and dose-response of photoreceptor Cell Degeneration in mouse retina after intravitreal injection of cobalt chloride were examined by conventional histological analysis by hematoxylin and eosin staining and in situ terminal dUTP-biotin nick end labeling of DNA fragments (TUNEL) method with the use of paraffin-embedded sections. The dose-response of photoreceptor Cell Degeneration in rat retina was also examined. Photoreceptor Cells progressively degenerated with time and under dose-response relationship. The suitable dose of cobalt chloride for the selective photoreceptor Cell Degeneration in mice is 10-12 nmol intravitreal injection at the volume of 2 microl. The retinal morphology of the mice 2 weeks after the 10-12 nmol intravitreal injection was similar to that of retinal Degeneration in the mutant rd mouse. Retinal damage of total retinal layers was induced by an excessive dose of cobalt chloride. The progression of retinal damage after cobalt chloride injection, measured morphologically, was completed at 1 week. However, nuclear DNA fragmentation, mainly detected at outer nuclear layer by TUNEL, peaked at 48 h after 12 nmol cobalt chloride injection. Thus, the selective photoreceptor Cell Degeneration induced by cobalt chloride follows DNA fragmentation at outer nuclear layer. The photoreceptor Cell Degeneration is established optionally by cobalt chloride without use of the retinal Degeneration mutant animals. Thus, we have described the development of a new model of retinal photoreceptor Cell Degeneration induced by a chemical hypoxia-mimicking agent.
Hideki Mori - One of the best experts on this subject based on the ideXlab platform.
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Localization of septin 8 in murine retina, and spatiotemporal expression of septin 8 in a murine model of photoreceptor Cell Degeneration.
Neuroscience letters, 2007Co-Authors: Akira Hara, Masayuki Niwa, Hitomi Aoki, Takahiro Kunisada, Ayako Taguchi, Yasuhiro Yamada, Hidenori Ito, Koh-ichi Nagata, Hideki MoriAbstract:The septins, which form a conserved family of cytoskeletal GTP-binding proteins in mammals, comprise stable heteromeric complexes and have diverse roles in protein scaffolding, cytokinesis, vesicle trafficking and plasma membrane integrity following Cell division. The goal of this study was to determine the localization of septin 8 in murine adult retina, and analyze the spatiotemporal expression of septin 8 in a murine model of photoreceptor Cell Degeneration. Expression of septin 8 in the normal retina of mouse and rat was observed by using immunohistochemistry and Western blotting. Furthermore, time course of the expression of septin 8 in mouse photoreceptor Cell Degeneration were examined by immunohistochemistry combined with hematoxylin and eosin staining, and in situ DNA fragment labeling method. In normal mouse and rat retina, localization of septin 8 is restricted in nuclei of photoreceptor Cells. 96 h after intravitreal injection of cobalt chloride most photoreceptor Cells lost septin 8 immunostaining at the same time as nuclear DNA fragmentation. The results of this study show that septin 8 protein is present in the specific location within the retina. Furthermore, the disappearance of septin 8 in the nuclei of photoreceptor Cells is concomitant with nuclear DNA fragmentation. This suggests that loss of septin 8 could be a useful prognostic indicator for photoreceptor Cell Degeneration.
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A new model of retinal photoreceptor Cell Degeneration induced by a chemical hypoxia-mimicking agent, cobalt chloride.
Brain research, 2006Co-Authors: Akira Hara, Masayuki Niwa, Hitomi Aoki, Masako Kumada, Takahiro Kunisada, Takeru Oyama, Tetsuya Yamamoto, Osamu Kozawa, Hideki MoriAbstract:Retinal photoreceptor Cell Degeneration was induced by cobalt chloride, a chemical hypoxia-mimicking agent in rodents. Time course and dose-response of photoreceptor Cell Degeneration in mouse retina after intravitreal injection of cobalt chloride were examined by conventional histological analysis by hematoxylin and eosin staining and in situ terminal dUTP-biotin nick end labeling of DNA fragments (TUNEL) method with the use of paraffin-embedded sections. The dose-response of photoreceptor Cell Degeneration in rat retina was also examined. Photoreceptor Cells progressively degenerated with time and under dose-response relationship. The suitable dose of cobalt chloride for the selective photoreceptor Cell Degeneration in mice is 10-12 nmol intravitreal injection at the volume of 2 microl. The retinal morphology of the mice 2 weeks after the 10-12 nmol intravitreal injection was similar to that of retinal Degeneration in the mutant rd mouse. Retinal damage of total retinal layers was induced by an excessive dose of cobalt chloride. The progression of retinal damage after cobalt chloride injection, measured morphologically, was completed at 1 week. However, nuclear DNA fragmentation, mainly detected at outer nuclear layer by TUNEL, peaked at 48 h after 12 nmol cobalt chloride injection. Thus, the selective photoreceptor Cell Degeneration induced by cobalt chloride follows DNA fragmentation at outer nuclear layer. The photoreceptor Cell Degeneration is established optionally by cobalt chloride without use of the retinal Degeneration mutant animals. Thus, we have described the development of a new model of retinal photoreceptor Cell Degeneration induced by a chemical hypoxia-mimicking agent.
Masayuki Niwa - One of the best experts on this subject based on the ideXlab platform.
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Retinal Cell Degeneration in Animal Models
International journal of molecular sciences, 2016Co-Authors: Masayuki Niwa, Hitomi Aoki, Akihiro Hirata, Hiroyuki Tomita, Paul G. Green, Akira HaraAbstract:The aim of this review is to provide an overview of various retinal Cell Degeneration models in animal induced by chemicals (N-methyl-d-aspartate- and CoCl2-induced), autoimmune (experimental autoimmune encephalomyelitis), mechanical stress (optic nerve crush-induced, light-induced) and ischemia (transient retinal ischemia-induced). The target regions, pathology and proposed mechanism of each model are described in a comparative fashion. Animal models of retinal Cell Degeneration provide insight into the underlying mechanisms of the disease, and will facilitate the development of novel effective therapeutic drugs to treat retinal Cell damage.
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Localization of septin 8 in murine retina, and spatiotemporal expression of septin 8 in a murine model of photoreceptor Cell Degeneration.
Neuroscience letters, 2007Co-Authors: Akira Hara, Masayuki Niwa, Hitomi Aoki, Takahiro Kunisada, Ayako Taguchi, Yasuhiro Yamada, Hidenori Ito, Koh-ichi Nagata, Hideki MoriAbstract:The septins, which form a conserved family of cytoskeletal GTP-binding proteins in mammals, comprise stable heteromeric complexes and have diverse roles in protein scaffolding, cytokinesis, vesicle trafficking and plasma membrane integrity following Cell division. The goal of this study was to determine the localization of septin 8 in murine adult retina, and analyze the spatiotemporal expression of septin 8 in a murine model of photoreceptor Cell Degeneration. Expression of septin 8 in the normal retina of mouse and rat was observed by using immunohistochemistry and Western blotting. Furthermore, time course of the expression of septin 8 in mouse photoreceptor Cell Degeneration were examined by immunohistochemistry combined with hematoxylin and eosin staining, and in situ DNA fragment labeling method. In normal mouse and rat retina, localization of septin 8 is restricted in nuclei of photoreceptor Cells. 96 h after intravitreal injection of cobalt chloride most photoreceptor Cells lost septin 8 immunostaining at the same time as nuclear DNA fragmentation. The results of this study show that septin 8 protein is present in the specific location within the retina. Furthermore, the disappearance of septin 8 in the nuclei of photoreceptor Cells is concomitant with nuclear DNA fragmentation. This suggests that loss of septin 8 could be a useful prognostic indicator for photoreceptor Cell Degeneration.
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A new model of retinal photoreceptor Cell Degeneration induced by a chemical hypoxia-mimicking agent, cobalt chloride.
Brain research, 2006Co-Authors: Akira Hara, Masayuki Niwa, Hitomi Aoki, Masako Kumada, Takahiro Kunisada, Takeru Oyama, Tetsuya Yamamoto, Osamu Kozawa, Hideki MoriAbstract:Retinal photoreceptor Cell Degeneration was induced by cobalt chloride, a chemical hypoxia-mimicking agent in rodents. Time course and dose-response of photoreceptor Cell Degeneration in mouse retina after intravitreal injection of cobalt chloride were examined by conventional histological analysis by hematoxylin and eosin staining and in situ terminal dUTP-biotin nick end labeling of DNA fragments (TUNEL) method with the use of paraffin-embedded sections. The dose-response of photoreceptor Cell Degeneration in rat retina was also examined. Photoreceptor Cells progressively degenerated with time and under dose-response relationship. The suitable dose of cobalt chloride for the selective photoreceptor Cell Degeneration in mice is 10-12 nmol intravitreal injection at the volume of 2 microl. The retinal morphology of the mice 2 weeks after the 10-12 nmol intravitreal injection was similar to that of retinal Degeneration in the mutant rd mouse. Retinal damage of total retinal layers was induced by an excessive dose of cobalt chloride. The progression of retinal damage after cobalt chloride injection, measured morphologically, was completed at 1 week. However, nuclear DNA fragmentation, mainly detected at outer nuclear layer by TUNEL, peaked at 48 h after 12 nmol cobalt chloride injection. Thus, the selective photoreceptor Cell Degeneration induced by cobalt chloride follows DNA fragmentation at outer nuclear layer. The photoreceptor Cell Degeneration is established optionally by cobalt chloride without use of the retinal Degeneration mutant animals. Thus, we have described the development of a new model of retinal photoreceptor Cell Degeneration induced by a chemical hypoxia-mimicking agent.
Hitomi Aoki - One of the best experts on this subject based on the ideXlab platform.
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Retinal Cell Degeneration in Animal Models
International journal of molecular sciences, 2016Co-Authors: Masayuki Niwa, Hitomi Aoki, Akihiro Hirata, Hiroyuki Tomita, Paul G. Green, Akira HaraAbstract:The aim of this review is to provide an overview of various retinal Cell Degeneration models in animal induced by chemicals (N-methyl-d-aspartate- and CoCl2-induced), autoimmune (experimental autoimmune encephalomyelitis), mechanical stress (optic nerve crush-induced, light-induced) and ischemia (transient retinal ischemia-induced). The target regions, pathology and proposed mechanism of each model are described in a comparative fashion. Animal models of retinal Cell Degeneration provide insight into the underlying mechanisms of the disease, and will facilitate the development of novel effective therapeutic drugs to treat retinal Cell damage.
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Localization of septin 8 in murine retina, and spatiotemporal expression of septin 8 in a murine model of photoreceptor Cell Degeneration.
Neuroscience letters, 2007Co-Authors: Akira Hara, Masayuki Niwa, Hitomi Aoki, Takahiro Kunisada, Ayako Taguchi, Yasuhiro Yamada, Hidenori Ito, Koh-ichi Nagata, Hideki MoriAbstract:The septins, which form a conserved family of cytoskeletal GTP-binding proteins in mammals, comprise stable heteromeric complexes and have diverse roles in protein scaffolding, cytokinesis, vesicle trafficking and plasma membrane integrity following Cell division. The goal of this study was to determine the localization of septin 8 in murine adult retina, and analyze the spatiotemporal expression of septin 8 in a murine model of photoreceptor Cell Degeneration. Expression of septin 8 in the normal retina of mouse and rat was observed by using immunohistochemistry and Western blotting. Furthermore, time course of the expression of septin 8 in mouse photoreceptor Cell Degeneration were examined by immunohistochemistry combined with hematoxylin and eosin staining, and in situ DNA fragment labeling method. In normal mouse and rat retina, localization of septin 8 is restricted in nuclei of photoreceptor Cells. 96 h after intravitreal injection of cobalt chloride most photoreceptor Cells lost septin 8 immunostaining at the same time as nuclear DNA fragmentation. The results of this study show that septin 8 protein is present in the specific location within the retina. Furthermore, the disappearance of septin 8 in the nuclei of photoreceptor Cells is concomitant with nuclear DNA fragmentation. This suggests that loss of septin 8 could be a useful prognostic indicator for photoreceptor Cell Degeneration.
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A new model of retinal photoreceptor Cell Degeneration induced by a chemical hypoxia-mimicking agent, cobalt chloride.
Brain research, 2006Co-Authors: Akira Hara, Masayuki Niwa, Hitomi Aoki, Masako Kumada, Takahiro Kunisada, Takeru Oyama, Tetsuya Yamamoto, Osamu Kozawa, Hideki MoriAbstract:Retinal photoreceptor Cell Degeneration was induced by cobalt chloride, a chemical hypoxia-mimicking agent in rodents. Time course and dose-response of photoreceptor Cell Degeneration in mouse retina after intravitreal injection of cobalt chloride were examined by conventional histological analysis by hematoxylin and eosin staining and in situ terminal dUTP-biotin nick end labeling of DNA fragments (TUNEL) method with the use of paraffin-embedded sections. The dose-response of photoreceptor Cell Degeneration in rat retina was also examined. Photoreceptor Cells progressively degenerated with time and under dose-response relationship. The suitable dose of cobalt chloride for the selective photoreceptor Cell Degeneration in mice is 10-12 nmol intravitreal injection at the volume of 2 microl. The retinal morphology of the mice 2 weeks after the 10-12 nmol intravitreal injection was similar to that of retinal Degeneration in the mutant rd mouse. Retinal damage of total retinal layers was induced by an excessive dose of cobalt chloride. The progression of retinal damage after cobalt chloride injection, measured morphologically, was completed at 1 week. However, nuclear DNA fragmentation, mainly detected at outer nuclear layer by TUNEL, peaked at 48 h after 12 nmol cobalt chloride injection. Thus, the selective photoreceptor Cell Degeneration induced by cobalt chloride follows DNA fragmentation at outer nuclear layer. The photoreceptor Cell Degeneration is established optionally by cobalt chloride without use of the retinal Degeneration mutant animals. Thus, we have described the development of a new model of retinal photoreceptor Cell Degeneration induced by a chemical hypoxia-mimicking agent.
James Edwards Morgan - One of the best experts on this subject based on the ideXlab platform.
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retina ganglion Cell Degeneration in glaucoma an opportunity missed a review
Clinical and Experimental Ophthalmology, 2012Co-Authors: James Edwards MorganAbstract:Retinal ganglion Cell Degeneration has been reported in a range of experimental models of glaucoma. Manifest as pruning of retinal ganglion Cell dendrites, it is likely to influence both the function and viability of affected Cells. Electrophysiological studies in primate glaucoma have shown that affected Cells retain some function and could therefore form a neural substrate for the recovery of visual function in glaucoma. Clinical studies in which the intraocular pressure is reduced have suggested that some improvement in retinal function may be possible in hypotensive eyes. These experimental studies highlight the importance of establishing the extent to which retinal ganglion Cell Degeneration occurs in human glaucoma. If substantial numbers of degenerating retinal ganglion Cells are present in glaucoma, they could present an ideal target for the recovery of vision.