Identification of Protein Kinase C Isoforms Involved in Type 1 Diabetic Encephalopathy in Mice

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, strepto...

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Main Authors: Jiayin Zheng, Yue Wang, Song Han, Yanlin Luo, Xiuli Sun, Ning Zhu, Li Zhao, Junfa Li
Format: Article
Language:English
Published: Wiley 2018-01-01
Series:Journal of Diabetes Research
Online Access:http://dx.doi.org/10.1155/2018/8431249
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author Jiayin Zheng
Yue Wang
Song Han
Yanlin Luo
Xiuli Sun
Ning Zhu
Li Zhao
Junfa Li
author_facet Jiayin Zheng
Yue Wang
Song Han
Yanlin Luo
Xiuli Sun
Ning Zhu
Li Zhao
Junfa Li
author_sort Jiayin Zheng
collection DOAJ
description 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 cPKCβII, nPKCε, and cPKCγ did not change in the hippocampus, cortex, and striatum at 2 and 8 weeks after STZ injection. The nPKCε 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, cPKCβII translocation to the membrane was significantly decreased in the cortex and hippocampus at 8 weeks after STZ injection. The translocation of cPKCγ 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 cPKCγ aggravated the impairment of spatial learning and memory. In conclusion, our results suggest that the decrease in the activity of cPKCβII and cPKCγ, especially cPKCγ, may play key roles in the pathogenesis of diabetic encephalopathy.
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series Journal of Diabetes Research
spelling doaj-art-e13aadda9856451494ced39f1d680b382025-02-03T07:24:21ZengWileyJournal of Diabetes Research2314-67452314-67532018-01-01201810.1155/2018/84312498431249Identification of Protein Kinase C Isoforms Involved in Type 1 Diabetic Encephalopathy in MiceJiayin Zheng0Yue Wang1Song Han2Yanlin Luo3Xiuli Sun4Ning Zhu5Li Zhao6Junfa Li7Department of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing 100069, ChinaDepartment of Neurology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, ChinaDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing 100069, ChinaDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing 100069, ChinaDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing 100069, ChinaDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing 100069, ChinaDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing 100069, ChinaDepartment of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing 100069, ChinaDiabetic 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 cPKCβII, nPKCε, and cPKCγ did not change in the hippocampus, cortex, and striatum at 2 and 8 weeks after STZ injection. The nPKCε 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, cPKCβII translocation to the membrane was significantly decreased in the cortex and hippocampus at 8 weeks after STZ injection. The translocation of cPKCγ 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 cPKCγ aggravated the impairment of spatial learning and memory. In conclusion, our results suggest that the decrease in the activity of cPKCβII and cPKCγ, especially cPKCγ, may play key roles in the pathogenesis of diabetic encephalopathy.http://dx.doi.org/10.1155/2018/8431249
spellingShingle Jiayin Zheng
Yue Wang
Song Han
Yanlin Luo
Xiuli Sun
Ning Zhu
Li Zhao
Junfa Li
Identification of Protein Kinase C Isoforms Involved in Type 1 Diabetic Encephalopathy in Mice
Journal of Diabetes Research
title Identification of Protein Kinase C Isoforms Involved in Type 1 Diabetic Encephalopathy in Mice
title_full Identification of Protein Kinase C Isoforms Involved in Type 1 Diabetic Encephalopathy in Mice
title_fullStr Identification of Protein Kinase C Isoforms Involved in Type 1 Diabetic Encephalopathy in Mice
title_full_unstemmed Identification of Protein Kinase C Isoforms Involved in Type 1 Diabetic Encephalopathy in Mice
title_short Identification of Protein Kinase C Isoforms Involved in Type 1 Diabetic Encephalopathy in Mice
title_sort identification of protein kinase c isoforms involved in type 1 diabetic encephalopathy in mice
url http://dx.doi.org/10.1155/2018/8431249
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