Kim Y H, Kim Y S, Kang S S, Noh H S, Kim H J, Cho G J, Choi W S
Department of Anatomy and Neurobiology, College of Medicine, Institute of Health Science, Gyeongsang National University, Jinju, South Korea.
Diabetologia. 2005 Jul;48(7):1411-5. doi: 10.1007/s00125-005-1774-7. Epub 2005 May 21.
AIMS/HYPOTHESIS: The present study aimed to investigate the expression levels of and the relationship between 14-3-3 zeta and protein kinase C (PKC) in the retina of early diabetes.
Changes in the expression levels of, and interaction between, 14-3-3 zeta and PKC were investigated by Northern and Western blot analyses, immunoprecipitation and double immunostaining in the retina of diabetic rats after 6 weeks of diabetes. PKC activity was examined using a PKC assay.
In the diabetic retina, the molecular levels of 14-3-3 zeta were reduced, while those of PKC beta and zeta were increased. Direct interaction between 14-3-3 zeta and PKC was markedly decreased in the retina after 6 weeks of diabetes, while PKC activity was increased.
CONCLUSIONS/INTERPRETATION: These findings show that a reduction in 14-3-3 zeta can induce PKC activation, suggesting that this is a main cause of visual dysfunction in the retina during diabetes.
目的/假设：本研究旨在调查早期糖尿病视网膜中14-3-3ζ与蛋白激酶C（PKC）的表达水平及其之间的关系。
通过Northern印迹和Western印迹分析、免疫沉淀以及双免疫染色，研究糖尿病6周后糖尿病大鼠视网膜中14-3-3ζ与PKC的表达水平变化及其相互作用。使用PKC检测法检测PKC活性。
在糖尿病视网膜中，14-3-3ζ的分子水平降低，而PKCβ和ζ的分子水平升高。糖尿病6周后，视网膜中14-3-3ζ与PKC之间的直接相互作用显著降低，而PKC活性增加。
结论/解读：这些发现表明14-3-3ζ的减少可诱导PKC激活，提示这是糖尿病期间视网膜视觉功能障碍的主要原因。
