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jun-B gene expression in rat retinal cells following focal retinal injury

K Ohki, Kazuhiko Yoshida, A. Yamakawa, Takayuki Harada, Hidehiko Matsuda, Junko Imaki

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Abstract

We examined jun-B gene expression in the rat retina after a focal retinal injury by in situ hybridization. 30 min after producing a penetrating retinal wound, the retina showed the expression of jun-B mRNA intensively in the inner nuclear layer (INL) and relatively sparsely in the ganglion cell layer. The double-labeled retina by immunocytochemistry and in situ hybridization demonstrated that jun-B mRNA within the INL surrounded S-100 protein immunoreactive cytoplasm in the middle sublayer of the INL. These results suggest that the jun-B expression is induced mainly in Müller cells following retinal damage.

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What this paper is about

We examined jun-B gene expression in the rat retina after a focal retinal injury by in situ hybridization. 30 min after producing a penetrating retinal wound, the retina showed the expression of jun-B mRNA intensively in the inner nuclear layer (INL) and relatively sparsely in the ganglion cell layer. The double-labeled retina by immunocytochemistry and in situ hybridization demonstrated that jun-B mRNA within the INL surrounded S-100 protein immunoreactive cytoplasm in the middle sublayer of the INL. These results suggest that the jun-B expression is induced mainly in Müller cells following retinal damage.

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Available abstract

We examined jun-B gene expression in the rat retina after a focal retinal injury by in situ hybridization. 30 min after producing a penetrating retinal wound, the retina showed the expression of jun-B mRNA intensively in the inner nuclear layer (INL) and relatively sparsely in the ganglion cell layer. The double-labeled retina by immunocytochemistry and in situ hybridization demonstrated that jun-B mRNA within the INL surrounded S-100 protein immunoreactive cytoplasm in the middle sublayer of the INL. These results suggest that the jun-B expression is induced mainly in Müller cells following retinal damage.

Key concepts: Inner nuclear layer, Retina, In situ hybridization, Ganglion cell layer, Retinal, Biology, Immunocytochemistry, Gene expression

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