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Identification of Protein Kinase C Isoforms Involved in Type 1 Diabetic Encephalopathy in Mice
Jiayin Zheng1, Yue Wang2, Song Han1
1Department of Neurobiology and Center of Stroke, Beijing Institute for Brain Disorders, Capital Medical University, Beijing 100069, China.
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 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.
Insights
Diabetic encephalopathy impairs cognitive function. This study shows reduced Protein Kinase C gamma (PKCγ) activity in the brain contributes to this condition, highlighting PKCγ as a potential therapeutic target.
Area of Science:
- Neuroscience
- Endocrinology
- Biochemistry
Background:
- Diabetic encephalopathy, a cognitive complication of diabetes mellitus, has unclear underlying mechanisms.
- Protein Kinase C (PKC) isoforms are implicated in diabetic complications but their role in diabetic encephalopathy is under-investigated.
Purpose of the Study:
- To investigate the role of specific Protein Kinase C (PKC) isoforms in the pathogenesis of diabetic encephalopathy.
- To examine the expression and activation of PKCβII, PKCε, and PKCγ in the brain during streptozotocin-induced diabetes.
Main Methods:
- Streptozotocin (STZ) was used to induce diabetes in mice.
- Cognitive function was assessed using the Morris water maze test.
- Expression and membrane translocation of PKC isoforms in the hippocampus, cortex, and striatum were analyzed.
Main Results:
- STZ-induced diabetic mice exhibited learning and memory deficits.
- While PKCε expression and translocation remained unchanged, cPKCβII translocation decreased in the cortex and hippocampus.
- cPKCγ translocation was significantly reduced in the hippocampus, cortex, and striatum; its genetic deletion worsened cognitive impairment.
Conclusions:
- Reduced activity of cPKCβII and particularly cPKCγ is strongly associated with the development of diabetic encephalopathy.
- These findings suggest that decreased PKCγ activity plays a critical role in the neuropathology of diabetes.
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