Nonperfusion of retina and choroid in transgenic mouse models of sickle cell disease.
Nonperfusion of retina and choroid in transgenic mouse models of sickle cell disease.
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镰状细胞病转基因小鼠模型中视网膜和脉络膜无灌注。
DOI：
10.1080/02713689808951225
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发表时间：
1998
影响因子：
2
通讯作者：
Nagel,RL
中科院分区：
文献类型：
--
作者：
Lutty,GA;Merges,C;McLeod,DS;Wajer,SD;Suzuka,SM;Fabry,ME;Nagel,RL
目的.确定血管阻塞和无灌注是否与镰状细胞病的αHβS[βMDD]和αHβS[αMDβMDD]转基因小鼠模型中发生的外部视网膜萎缩、视网膜病变和脉络膜病变（脉络膜视网膜病变）相关。将表达高水平人β球蛋白的αHβS[βMDD]和αHβS[αMDβMDD]转基因小鼠系的小鼠麻醉，并心内给予辣根过氧化物酶（HRP）。1分钟后，处死动物，切除一只眼睛的视网膜，固定，并在二氨基联苯胺（DAB）中显影。对侧眼固定，甲基丙烯酸乙二醇酯包埋，2.5 μm切片显色。HRP反应产物（HRP-RP）和染色的红细胞（RBC）（由于内源性过氧化物酶）弥漫性分布在对照动物（小鼠β Major缺失纯合子，不表达β S转基因）的平贴视网膜的所有血管腔内。在42.5%的表达β S的转基因小鼠中，没有任何增殖性视网膜病变，许多血管含有红细胞栓，并且缺乏内腔HRP-RP。除了红细胞堆积外，有时在闭塞部位还存在纤维蛋白。在同一动物的整只眼睛切片中，感光细胞变性的病灶与脉络膜毛细血管非灌注区（缺乏HRP-PR的管腔）相关。在感光细胞正常的区域，脉络膜毛细血管出现灌注（HRP-RP存在）。在增生性脉络膜视网膜病变的动物中，一些新生血管形成缺乏管腔HRP-RP，提示自体梗死。在无视网膜和脉络膜新生血管的αHβS[βMDD]和αHβS[αMDβMDD]系小鼠中观察到非灌注视网膜和脉络膜血管，而所有新生血管的小鼠均有非灌注区域。此外，PR丢失的小病灶与非灌注的脉络膜毛细血管区相关。这些结果表明，镰状细胞介导的血管闭塞是在这些模型中发生的脉络膜视网膜病变和外视网膜萎缩的初始事件。Curr. 17：438-444，1998.
Purpose. To determine if vascular occlusion and nonperfusion is associated with the outer retinal atrophy, retinopathy, and choroidopathy (chorioretinopathy) that occurs in the αHβS[βMDD] and αHβS[αMDβMDD] transgenic mouse models of sickle cell disease.Methods. Mice from the αHβS[βMDD] and αHβS[αMDβMDD] transgenic mouse lines that express high levels of human βSglobin were anesthetized and administered horseradish peroxidase (HRP) intracardially. After 1 min, the animals were sacrificed, and the retina from one eye was excised, fixed, and developed in diaminobenzidine (DAB). The contralateral eye was fixed, embedded whole in glycol methacrylate, and HRP developed in 2.5 μm sections.Results. HRP reaction product (HRP-RP) and stained erythrocytes (RBCs) (due to endogenous peroxidase) were diffusely distributed within all vascular lumens in fiatmount retinas from control animals (littermates homozygous for the mouse βMajordeletion not expressing the βStransgene). In 42.5% of the transgenic mice expressing βSwithout any proliferative retinopathy, many blood vessels contained RBC plugs and lacked lumenal HRP-RP. In addition to packed RBCs, fibrin was sometimes present at sites of occlusion. In sections from whole eyes of the same animals, foci of photoreceptor degeneration were associated with areas of choriocapillaris nonperfusion (lumen that lacked HRP-PR). In areas with normal photoreceptors, the choriocapillaris appeared perfused (HRP-RP was present). In animals with proliferative chorioretinopathy, some neovascular formations lacked luminal HRP-RP, suggesting autoinfarction.Conclusions. Nonperfused retinal and choroidal vessels were observed in mice from the αHβS[βMDD] and αHβS[αMDβMDD] lines without retinal and choroidal neovascularization, whereas, all mice with neovascularization had nonperfused areas. Furthermore, small foci of PR loss were associated with areas of nonperfused choriocapillaris. These results suggest that sickle cell-mediated vaso-occlusions are an initial event in the chorioretinopathy and outer retinal atrophy that occurs in these models. Curr. Eye Res. 17: 438–444, 1998.
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DOI：
--
发表时间：
1987
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1978
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DOI：
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发表时间：
1976
期刊：
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DOI：
10.1136/bjo.67.2.107
发表时间：
1983
期刊：
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