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A novel role for the calcium sensing receptor in rat diabetic encephalopathy
Shiyun Dong1, Gang Li, Dan Zheng
1Department of Pathophysiology, Harbin Medical University, Harbin, China.
Background:
Diabetic encephalopathy is a common complication of diabetes, and it may be involved in altering intracellular calcium concentrations ([Ca(2+)]i) at its onset. The calcium sensing receptor (CaSR) is a G-protein coupled receptor, however, the functional involvement of CaSR in diabetic encephalopathy remains unclear.
Methods:
In this study, diabetic rats were modeled by STZ (50 mg/kg). At the end of 4, 8 and 12 weeks, the CaSR expression in hippocampus was analyzed by Western blot. In neonatal rat hippocampal neurons, the [Ca(2+)]i was detected by laser scanning confocal microscopy, the production of reactive oxygen species (ROS) in mitochondria, the level of NO and the mitochondrial transmembrane potential were measured by MitoSOX, DAF-FM and JC-1, respectively.
Results:
Our results showed in hippocampal neurons treated with high glucose, CaSR regulated [Ca(2+)]i through the PLC-IP3 pathway. CaSR expression was decreased and was involved in the changes in [Ca(2+)]i. Mitochondrial membrane potential, NO release and expression of p-eNOS decreased, while the production of ROS in mitochondria increased.
Conclusion:
Down-regulation of CaSR expression was accompanied by neuronal injury, calcium disturbance, increased ROS production and decreased release of NO. Up-regulation of CaSR expression attenuated these changes through a positive compensatory protective mechanism to inhibit and delay diabetic encephalopathy in rats.
Insights
Diabetic encephalopathy involves altered intracellular calcium. This study shows calcium sensing receptor (CaSR) down-regulation worsens neuronal injury, while up-regulation offers protection against diabetic encephalopathy.
Area of Science:
- Neuroscience
- Endocrinology
- Cell Biology
Background:
- Diabetic encephalopathy is a complication of diabetes.
- Altered intracellular calcium concentrations ([Ca(2+)]i) are implicated in diabetic encephalopathy.
- The role of the calcium sensing receptor (CaSR) in this condition is unclear.
Purpose of the Study:
- To investigate the functional involvement of CaSR in diabetic encephalopathy.
- To elucidate the mechanisms by which CaSR affects neuronal function in diabetes.
Main Methods:
- Diabetic rat models were induced using streptozotocin (STZ).
- CaSR expression in the hippocampus was analyzed via Western blot.
- Intracellular calcium ([Ca(2+)]i), mitochondrial reactive oxygen species (ROS), nitric oxide (NO) levels, and mitochondrial membrane potential were measured in hippocampal neurons.
Main Results:
- High glucose conditions in hippocampal neurons showed CaSR regulating [Ca(2+)]i via the PLC-IP3 pathway.
- Decreased CaSR expression correlated with altered [Ca(2+)]i, reduced mitochondrial membrane potential, decreased NO release, and increased mitochondrial ROS production.
- These changes are associated with neuronal injury.
Conclusions:
- Down-regulation of CaSR expression contributes to neuronal injury, calcium disturbance, increased ROS, and decreased NO release in diabetic encephalopathy.
- Up-regulation of CaSR expression demonstrated a compensatory protective effect, inhibiting and delaying the progression of diabetic encephalopathy in rats.
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