A Novel Role for the Calcium Sensing Receptor in Rat Diabetic Encephalopathy
Background: Diabetic encephalopathy is a common complication of diabetes, and it may be involved in altering intracellular calcium concentrations ([Ca2+]i) at its onset. The calcium sensing receptor (CaSR) is a G-protein coupled receptor, however, the functional involvement of CaSR in diabetic encep...
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| Format: | Article |
| Language: | English |
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Cell Physiol Biochem Press GmbH & Co KG
2015-01-01
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| Series: | Cellular Physiology and Biochemistry |
| Subjects: | |
| Online Access: | http://www.karger.com/Article/FullText/369673 |
| _version_ | 1818341723882913792 |
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| author | Shiyun Dong Gang Li Dan Zheng Jichao Wu Dianjun Sun Fan Yang Xiangjing Yu Ting Li Aili Sun Jiaqi Liu Xin Zhong Changqing Xu Fanghao Lu Weihua Zhang |
| author_facet | Shiyun Dong Gang Li Dan Zheng Jichao Wu Dianjun Sun Fan Yang Xiangjing Yu Ting Li Aili Sun Jiaqi Liu Xin Zhong Changqing Xu Fanghao Lu Weihua Zhang |
| author_sort | Shiyun Dong |
| collection | DOAJ |
| description | Background: Diabetic encephalopathy is a common complication of diabetes, and it may be involved in altering intracellular calcium concentrations ([Ca2+]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 [Ca2+]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 [Ca2+]i through the PLC-IP3 pathway. CaSR expression was decreased and was involved in the changes in [Ca2+]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. |
| first_indexed | 2024-12-13T16:03:20Z |
| format | Article |
| id | doaj.art-3a3a6953476a432f958773ee4dc4453c |
| institution | Directory Open Access Journal |
| issn | 1015-8987 1421-9778 |
| language | English |
| last_indexed | 2024-12-13T16:03:20Z |
| publishDate | 2015-01-01 |
| publisher | Cell Physiol Biochem Press GmbH & Co KG |
| record_format | Article |
| series | Cellular Physiology and Biochemistry |
| spelling | doaj.art-3a3a6953476a432f958773ee4dc4453c2022-12-21T23:39:06ZengCell Physiol Biochem Press GmbH & Co KGCellular Physiology and Biochemistry1015-89871421-97782015-01-01351385010.1159/000369673369673A Novel Role for the Calcium Sensing Receptor in Rat Diabetic EncephalopathyShiyun DongGang LiDan ZhengJichao WuDianjun SunFan YangXiangjing YuTing LiAili SunJiaqi LiuXin ZhongChangqing XuFanghao LuWeihua ZhangBackground: Diabetic encephalopathy is a common complication of diabetes, and it may be involved in altering intracellular calcium concentrations ([Ca2+]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 [Ca2+]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 [Ca2+]i through the PLC-IP3 pathway. CaSR expression was decreased and was involved in the changes in [Ca2+]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.http://www.karger.com/Article/FullText/369673Calcium sensing receptorDiabetic encephalopathy[Ca2+]iHigh glucose |
| spellingShingle | Shiyun Dong Gang Li Dan Zheng Jichao Wu Dianjun Sun Fan Yang Xiangjing Yu Ting Li Aili Sun Jiaqi Liu Xin Zhong Changqing Xu Fanghao Lu Weihua Zhang A Novel Role for the Calcium Sensing Receptor in Rat Diabetic Encephalopathy Cellular Physiology and Biochemistry Calcium sensing receptor Diabetic encephalopathy [Ca2+]i High glucose |
| title | A Novel Role for the Calcium Sensing Receptor in Rat Diabetic Encephalopathy |
| title_full | A Novel Role for the Calcium Sensing Receptor in Rat Diabetic Encephalopathy |
| title_fullStr | A Novel Role for the Calcium Sensing Receptor in Rat Diabetic Encephalopathy |
| title_full_unstemmed | A Novel Role for the Calcium Sensing Receptor in Rat Diabetic Encephalopathy |
| title_short | A Novel Role for the Calcium Sensing Receptor in Rat Diabetic Encephalopathy |
| title_sort | novel role for the calcium sensing receptor in rat diabetic encephalopathy |
| topic | Calcium sensing receptor Diabetic encephalopathy [Ca2+]i High glucose |
| url | http://www.karger.com/Article/FullText/369673 |
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