...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >Diabetes downregulates presynaptic proteins and reduces basal synapsin I phosphorylation in rat retina.
【24h】

Diabetes downregulates presynaptic proteins and reduces basal synapsin I phosphorylation in rat retina.

机译：糖尿病会下调大鼠视网膜中的突触前蛋白并减少基础突触蛋白I的磷酸化。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Diabetic retinopathy can result in vision loss and involves progressive neurovascular degeneration of the retina. This study tested the hypothesis that diabetes decreases the retinal expression of presynaptic proteins involved in synaptic function. The protein and mRNA contents for synapsin I, synaptophysin, vesicle-associated membrane protein 2, synaptosomal-associated protein of 25 kDa and postsynaptic density protein of 95 kDa were measured by immunohistochemistry, immunoblotting and real-time quantitative polymerase chain reaction in whole retinas and retinal synaptosomes from streptozotocin-diabetic and control Sprague-Dawley rats. There was less presynaptic protein immunoreactivity after 1 and 3 months of diabetes than in controls. Discrete synaptophysin-immunoreactive puncta were significantly smaller and fewer in sections from 1- and 3-month diabetic rat retinas than in those from controls. The content of presynaptic proteins was significantly less in whole retinas of 1- and 3-month diabetic rats, and in synaptosomes from 1-month diabetic rats, than in controls. Whole retinas had significantly less mRNA for these genes after 3 months but not 1 month of diabetes, as compared to controls (with the exception of postsynaptic density protein of 95 kDa). In contrast, there was significantly less mRNA for synaptic proteins in synaptosomes of 1-month diabetic rats than in controls, suggesting a localized depletion at synapses. Protein and mRNA for beta-actin and neuron-specific enolase were unchanged by diabetes. The ratio of phosphorylated to total synapsin I was also reduced in whole retina and isolated synaptosomes from 1-month diabetic rats, as compared to controls. These data suggest that diabetes has a profound impact on presynaptic protein expression in the retina, and may provide a mechanism for the well-established defects in vision and the electrophysiological response of the retina in diabetes.
机译：糖尿病性视网膜病可导致视力丧失，并涉及视网膜进行性神经血管变性。这项研究检验了以下假设：糖尿病会降低涉及突触功能的突触前蛋白的视网膜表达。通过免疫组织化学，免疫印迹和实时定量聚合酶链反应，分别检测了25kDa的突触素I，突触素，囊泡相关膜蛋白2，突触相关蛋白和95kDa的蛋白和mRNA含量。链脲佐菌素-糖尿病和对照Sprague-Dawley大鼠的视网膜突触小体。糖尿病1个月和3个月后，突触前蛋白的免疫反应性低于对照组。与对照组相比，在1个月和3个月糖尿病大鼠视网膜中，离散的突触素-免疫反应性小点明显更小且更少。与对照组相比，在1个月和3个月糖尿病大鼠的整个视网膜中以及在1个月糖尿病大鼠的突触小体中，突触前蛋白的含量均显着降低。与对照组相比，糖尿病3个月后但不是1个月时，整个视网膜的这些基因mRNA显着减少（突触后密度蛋白为95 kDa）。相反，与对照组相比，在1个月糖尿病大鼠的突触小体中，突触蛋白的mRNA明显少于对照组，这表明突触处有局部消耗。 β-肌动蛋白和神经元特异性烯醇化酶的蛋白质和mRNA在糖尿病中没有改变。与对照组相比，在1个月糖尿病大鼠的整个视网膜和分离的突触小体中，磷酸化的突触蛋白I与总突触蛋白I的比例也降低了。这些数据表明，糖尿病对视网膜中突触前蛋白的表达具有深远的影响，并可能为糖尿病中视力和视网膜的电生理反应中公认的缺陷提供一种机制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号