Expression of 14-3-3 ζ and interaction with protein kinase C in the rat retina in early diabetes

• Published in: Diabetologia 2005-07, Vol.48 (7), p.1411-1415
• Main Authors: KIRN, Y. H, KIM, Y. S, KANG, S. S, NOH, H. S, KIM, H. J, CHO, G. J, CHOI, W. S
• Format: Article
• Language: English
• Subjects: 14-3-3 Proteins - genetics; Animals; Biological and medical sciences; Blotting, Northern; Blotting, Western; Diabetes Mellitus, Experimental - enzymology; Diabetes Mellitus, Experimental - physiopathology; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Eye and associated structures. Visual pathways and centers. Vision; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation; Male; Medical sciences; Protein Kinase C - genetics; Rats; Rats, Sprague-Dawley; Retina - physiopathology; RNA, Messenger - genetics; Transcription, Genetic; Vertebrates: nervous system and sense organs
• ISSN: 0012-186X; 1432-0428
• DOI: 10.1007/s00125-005-1774-7

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. 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.