ClC-3 Expression and Its Association with Hyperglycemia Induced HT22 Hippocampal Neuronal Cell Apoptosis

Although apoptosis plays an important role in the development of Diabetic Encephalopathy (DE), the underlying molecular mechanisms remain unclear. With respect to this, the present work aims to study the variation in chloride/proton exchanger ClC-3 expression and its association with HT22 hippocampa...

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Bibliographic Details
Published in:Journal of diabetes research 2016-01, Vol.2016 (2016), p.1-12
Main Authors: Tu, Yanyang, Fu, Jianfang, Li, Qian, Wang, Zhen, Zhang, Pengxing, Liu, Hui, Ren, Dongni, Wang, Xin, Liu, Tao, Fan, Feiyan, Liu, Nan
Format: Article
Language:English
Subjects:
Animals
Antibodies
Apoptosis
Blotting, Western
Cell culture
Cell cycle
Cell Line
Cell Survival
Chloride
Chloride Channels - analysis
Chloride Channels - physiology
Diabetes
Flow Cytometry
Glucose
Hippocampus - pathology
Hyperglycemia
Hyperglycemia - pathology
Mice
Nitrobenzoates - pharmacology
Oxidative Stress
Proteins
Studies
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Summary:Although apoptosis plays an important role in the development of Diabetic Encephalopathy (DE), the underlying molecular mechanisms remain unclear. With respect to this, the present work aims to study the variation in chloride/proton exchanger ClC-3 expression and its association with HT22 hippocampal neuronal apoptosis under hyperglycemic condition in vitro. The cells were stimulated with added 0, 5, or 25 mM glucose or mannitol for up to 72 hours before assessing the rate of ClC-3 expression, cell viability, and apoptosis. In a consecutive experiment, cells received chloride channel blocker in addition to glucose. The rate of cellular death/apoptosis and viability was measured using Flow Cytometry and MTT assay, respectively. Changes in ClC-3 expression were assessed using immunofluorescence staining and western blot analysis. The results revealed a significant increase in cellular apoptosis and reduction in viability, associated with increased ClC-3 expression in high glucose group. Osmolarity had no role to play. Addition of chloride channel blocker completely abolished this effect. Thus we conclude that, with its increased expression, ClC-3 plays a major role in hyperglycemia induced hippocampal neuronal apoptosis. To strengthen our understanding of this aforesaid association, we conducted an extensive literature search which is presented in this paper.
ISSN:2314-6745
2314-6753
DOI:10.1155/2016/2984380