Retinal ion regulation in a mouse model of diabetic retinopathy: natural history and the effect of Cu/Zn superoxide dismutase overexpression.
Retinal ion regulation in a mouse model of diabetic retinopathy: natural history and the effect of Cu/Zn superoxide dismutase overexpression.
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DOI：
10.1167/iovs.08-2918
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发表时间：
2009-05
影响因子：
4.4
通讯作者：
Roberts R
中科院分区：
文献类型：
--
作者：
Berkowitz BA;Gradianu M;Bissig D;Kern TS;Roberts R
验证锰增强MRI（MEMRI）可用于评价野生型（WT）和Cu/Zn超氧化物歧化酶（SOD 1）过表达小鼠视网膜内离子失调的假设。根据光适应和暗适应WT C57 BL/6小鼠（以测量MEMRI对小鼠正常视觉处理的敏感性）以及暗适应糖尿病和非糖尿病WT和Cu/Zn超氧化物歧化酶过表达（SOD 1 OE）小鼠的高分辨率数据测量中央视网膜内离子活性和视网膜厚度。糖化血红蛋白和视网膜血管组织病理学也进行了测定。在WT小鼠中，与暗适应相比，光适应降低了视网膜外锰摄取，而对视网膜内锰摄取没有影响。在糖尿病WT小鼠中，视网膜内锰摄取在糖尿病发作的1.5至4个月之间变得低于正常，然后相对增加。用MEMRI测定的中央视网膜厚度在糖尿病小鼠中作为年龄的函数降低，但在对照小鼠中保持恒定。非糖尿病SOD 1 OE小鼠视网膜锰摄取正常，但视网膜厚度低于正常，脱细胞毛细血管密度高于正常。在糖尿病4.2个月时，SOD 1 OE小鼠的锰摄取正常，没有进一步变薄;糖尿病9至10个月时，无细胞毛细血管频率没有增加。在新发糖尿病视网膜病变中，MEMRI提供了对SOD 1过表达敏感的离子失调模式的分析测量。在该模型中，SOD 1过表达抑制视网膜异常的潜在益处受到独立于糖尿病发展的视网膜和血管变性的限制。
To test the hypotheses that manganese-enhanced MRI (MEMRI) is useful in evaluating intraretinal ion dysregulation in wild-type (WT) and Cu/Zn superoxide dismutase (SOD1) overexpressor mice. Central intraretinal ion activity and retinal thickness were measured from high-resolution data of light- and dark-adapted WT C57BL/6 mice (to gauge MEMRI sensitivity to normal visual processing in mice) and dark-adapted diabetic and nondiabetic WT and Cu/Zn superoxide dismutase overexpressor (SOD1OE) mice. Glycated hemoglobin and retinal vascular histopathology were also determined. In WT mice, light adaptation reduced outer retinal manganese uptake compared with that in dark adaptation; no effect on inner retinal uptake was found. In diabetic WT mice, intraretinal manganese uptake became subnormal between 1.5 and 4 months of diabetes onset and then relatively increased. Central retinal thickness, as determined with MEMRI, decreased as a function of age in diabetic mice but remained constant in control mice. Nondiabetic SOD1OE mice had normal retinal manganese uptake but subnormal retinal thickness and supernormal acellular capillary density. At 4.2 months of diabetes, SOD1OE mice had normal manganese uptake and no further thinning; acellular capillaries frequency did not increase by 9 to 10 months of diabetes. In emerging diabetic retinopathy, MEMRI provided an analytic measure of an ionic dysregulatory pattern that was sensitive to SOD1 overexpression. The potential benefit of SOD1 overexpression to inhibit retinal abnormality in this model is limited by the retinal and vascular degeneration that develops independently of diabetes.
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影响因子：
15.9
作者：
Barber, AJ;Lieth, E;Gardner, TW
通讯作者：
Gardner, TW
影响因子：
7.7
作者：
Kern, TS;Engerman, RL
通讯作者：
Engerman, RL
影响因子：
4.4
作者：
Berkowitz, Bruce A.;Roberts, Robin;Vingrys, Algis J.
通讯作者：
Vingrys, Algis J.
影响因子：
4.4
作者：
Berkowitz, Bruce A.;Roberts, Robin;Luan, Hongmei
通讯作者：
Luan, Hongmei
影响因子：
4.4
作者：
Berkowitz, Bruce A.;Roberts, Robin;Gradianu, Marius
通讯作者：
Gradianu, Marius