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S抗原在发育中的rds小鼠视网膜中的定位。

S-antigen localization in developing rds mouse retina.

作者信息

Sai S, Usukura J, Shinohara T, Wakabayashi T, Awaya S

机构信息

Department of Ophthalmology, Nagoya University, Japan.

出版信息

Jpn J Ophthalmol. 1992;36(3):331-41.

PMID:1464973
Abstract

The morphology of the photoreceptor cell and localization of the cytoplasmic soluble protein, S-antigen, in the retina of the developing retinal degeneration slow (rds) mutant mouse (2-505 postnatal days) were studied by improved immunocytochemical and freeze-substitution methods. Anti-S-antigen antibody labeling was observed first in the postnatal 10-day retina under light microscope. Labeling signals increased progressively to a maximum level in 20 days, and then decreased gradually to an undetectable level by 505 postnatal days. By electron microscopic immunocytochemical methods, S-antigen was detected first in the photoreceptor cells at 3 postnatal days, and increased with development. It was located in the entire cytoplasm of the photoreceptor cell including the rudimentary outer segment, but degenerated and disappeared by 505 postnatal days. S-antigen was also present in the membranous vesicles budding off from the photoreceptor membrane to the subretinal space. The rds photoreceptor cell seems to lose other soluble proteins together with these vesicles. From these results and other published data, we speculate that the degeneration of the photoreceptor cells may be the secondary effects of the loss of a large amount of soluble and membrane proteins following the malfunction of membrane. Recent reports show the rds mouse must have a gene defect in the membrane component such as peripherin or the 39 kDa protein.

摘要

采用改良的免疫细胞化学和冷冻置换方法,研究了发育性视网膜变性缓慢(rds)突变小鼠(出生后2 - 505天)视网膜中光感受器细胞的形态以及细胞质可溶性蛋白S抗原的定位。在光学显微镜下,出生后10天的视网膜中首次观察到抗S抗原抗体标记。标记信号在20天时逐渐增加至最高水平,然后逐渐下降,到出生后505天时降至检测不到的水平。通过电子显微镜免疫细胞化学方法,出生后3天在光感受器细胞中首次检测到S抗原,并随发育而增加。它位于光感受器细胞的整个细胞质中,包括未成熟的外段,但在出生后505天时退化并消失。S抗原也存在于从光感受器膜向视网膜下间隙出芽的膜泡中。rds光感受器细胞似乎与这些膜泡一起丢失了其他可溶性蛋白。根据这些结果和其他已发表的数据,我们推测光感受器细胞的退化可能是膜功能障碍后大量可溶性和膜蛋白丢失的继发效应。最近的报道表明,rds小鼠在膜成分如外周蛋白或39 kDa蛋白方面一定存在基因缺陷。

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