Akihiro Ohira

Experimental retinal tolerance to emulsified silicone oil.

Vitreous replacement by silicone oil has become increasingly popular in the treatment of severe and complicated retinal detachment. Several studies have suggested that silicone oil may be toxic to the retina or may stimulate periretinal proliferation. To better understand its effects, emulsified or nonemulsified silicone oil was injected into rabbit eyes that had undergone mechanical vitrectomy. Silicone oil was labeled with phthalocyanine blue to aid in histologic localization. Retinal changes were compared by light microscopy at 1, 4, and 12 weeks after intraocular injection. Emulsified silicone oil was found to penetrate the inner retina at 1 week and cause epiretinal membrane formation as early as 4 weeks after injection. Nonemulsified oil produced no histologic changes in the retina. No cytotoxic effects were observed in eyes treated with ether emulsified or nonemulsified silicone oil. It is concluded that emulsified silicone oil can both penetrate the retina and stimulate epiretinal membrane formation in the vitrectomized rabbit eye.

Changes in Manganese Superoxide Dismutase Expression After Exposure of the Retina to Intense Light

Manganese superoxide dismutase (Mn-SOD) is a naturally-occurring scavenger of superoxide, one of several reactive oxygen intermediates. To determine if Mn-SOD expression is enhanced as a defensive mechanism against oxidative challenges, such as intense light exposure, rats were exposed to cyclic light (80 lux) for 2 weeks, intense light (1,800 lux) for 24 h, and then again to cyclic light. Experimental and control (exposed to cyclic light only) eyes were enucleated 3 h, 1, 3, 7, and 14 days after light challenge. Protein expression was examined immunohistochemically using rabbit antisera against rat Mn-SOD. There was no significant difference between the light-exposed and the control groups in the thickness of the outer nuclear layers. Both retinal pigment epithelial cells and photoreceptor inner segments in the normal retina were labeled for Mn-SOD. Mn-SOD labeling was lost 3 h and day 1 after light challenge. It was re-expressed in the retinal pigment epithelial cells 3, 7, and 14 days after the light challenge, and in the photoreceptor inner segments after day 14. These results suggest that the retina might have a protective potential against light damage, in which Mn-SOD may play an important role.

Glial-, neuronal- and photoreceptor-specific cell markers in rosettes of retinoblastoma and retinal dysplasia

Previous studies have shown that a rosette formation represents an attempt to form embryonic retinal tissue, primarily rods and cones. To test the theories as to the origin and characteristics of retinoblastoma cells, we compared the characteristics of tumor rosettes with those of dysplastic rosettes seen in retinal dysplasia using the glial, neuronal and photoreceptor markers. Forty-four retinoblastoma and one retinal dysplasia specimens were analyzed by indirect immunohistochemistry, using specific antibodies against glial fibrillary acidic protein, S-100 protein, myelin basic protein, neuron-specific enolase, neurofilament, retinal S-antigen and retinal pigment epithelial antigen. In human retinoblastoma, all the glial, neuronal, retinal pigment epithelial, and photoreceptor cell markers, except for the neurofilament, were present in parts of rosette-forming tumor cells. However, their localization was different for each antigen and it was not clear whether each tumor cell possesses several antigens. These immuno-positive tumor cells were cytologically indistinguishable from other rosette-forming cells at the light microscopic level. In retinal dysplasia, neuron specific enolase and retinal S-antigen were diffusely expressed in the dysplastic rosettes, however, other antigen were not seen in those rosettes. The staining pattern by immunocytochemistry is totally different in tumor rosettes from dysplastic ones. We found varying localizations of different immunoreactivities within tumor rosettes. These results led us to suggest that tumor cells in the rosettes of retinoblastoma may have the ability to differentiate into neural and glial cells. To prove the theory that retinoblastoma cells may have originated from a primitive neuroectodermal cell capable of multipotentiality, further investigation is needed.

Localization and possible gene expression of proteoglycan decorin in the trabecular meshwork.

It is known that trabecular meshwork cells produce proteoglycans and that local production may be associated with aqueous outflow resistance. In an attempt to identify intraocular production of proteoglycan decorin in the anterior chamber angle of mammalian eyes, we conducted a Northern blot analysis and immunohistochemical studies. Northern blot analysis suggested gene expression of proteoglycan decorin in trabecular meshwork cells. Also, immunohistochemical studies using anti-decorin antibody demonstrated decorin-like immunoreactivity in the trabecular meshwork and around the Schlemms canal. Our data demonstrate the presence of proteoglycan decorin in the outflow pathway, suggesting that decorin is a component of extracellular matrices in these regions and may be associated with outflow resistance.