Identification of Protein Kinase C Isoforms Involved in Type 1 Diabetic Encephalopathy in Mice. (18th March 2018)

• Record Type: Journal Article
• Authors: Zheng, Jiayin; Wang, Yue; Han, Song; Luo, Yanlin; Sun, Xiuli; Zhu, Ning; Zhao, Li; Li, Junfa
• Other Names: Chattopadhyay Munmun Academic Editor.
• Is Part Of: Journal of diabetes research. Volume 2018(2018)
• Publication Date: 2018-03-18
• Subjects: Diabetes -- Periodicals; Diabetes -- Pathophysiology -- Periodicals; Diabetes -- Prevention -- Periodicals; Diabetes -- Etiology -- Periodicals; Diabetes -- Epidemiology -- Periodicals; Diabetes -- Pathogenesis -- Periodicals; 616.462005
• DOI: 10.1155/2018/8431249
• Languages: English
• ISSNs: 2314-6745

Abstract

Abstract : Diabetic encephalopathy is a complication of diabetes mellitus characterized by impaired cognitive functions. Protein kinase C (PKC) isoforms are rarely reported on diabetic encephalopathy, although they have been believed to play crucial roles in other diabetic complications. In this study, streptozotocin- (STZ-) induced diabetic mice were found to exhibit learning and memory deficits in the Morris water maze test. Meanwhile, the expression of cPKC β II, nPKC ε, and cPKC γ did not change in the hippocampus, cortex, and striatum at 2 and 8 weeks after STZ injection. The nPKC ε translocation to the membrane, where it is activated, was not altered in the above brain regions at 2 and 8 weeks after STZ injection. Nevertheless, cPKC β II translocation to the membrane was significantly decreased in the cortex and hippocampus at 8 weeks after STZ injection. The translocation of cPKC γ from the cytosol to the membrane was remarkably decreased in the hippocampus at 2 and 8 weeks and in the cortex and striatum at 8 weeks after STZ injection. In addition, deletion of cPKC γ aggravated the impairment of spatial learning and memory. In conclusion, our results suggest that the decrease in the activity of cPKC β II and cPKC γ, especially cPKC γ, may play key roles in the pathogenesis of diabetic encephalopathy.