Fluid Retention Caused by Rosiglitazone Is Related to Increases in AQP2 and αENaC Membrane Expression
Peroxisome proliferator activated receptor-γ (PPARγ) is a ligand-activated transcription factor of the nuclear hormone receptor superfamily. The decreased phosphorylation of PPARγ due to rosiglitazone (ROS) is the main reason for the increased insulin sensitivity caused by this antidiabetic drug. Ho...
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| Format: | Article |
| Language: | English |
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Wiley
2017-01-01
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| Series: | PPAR Research |
| Online Access: | http://dx.doi.org/10.1155/2017/8130968 |
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| author | Jinghua Xu Mingyue Pan Xiaoli Wang Lishi Xu Lanfang Li Cheng Xu |
| author_facet | Jinghua Xu Mingyue Pan Xiaoli Wang Lishi Xu Lanfang Li Cheng Xu |
| author_sort | Jinghua Xu |
| collection | DOAJ |
| description | Peroxisome proliferator activated receptor-γ (PPARγ) is a ligand-activated transcription factor of the nuclear hormone receptor superfamily. The decreased phosphorylation of PPARγ due to rosiglitazone (ROS) is the main reason for the increased insulin sensitivity caused by this antidiabetic drug. However, there is no clear evidence whether the nuclear translocation of p-PPARγ stimulated by ROS is related to fluid retention. It is also unclear whether the translocation of p-PPARγ is associated with the change of aquaporin-2 (AQP2) and epithelial sodium channel α subunit (αENaC) in membranes, cytoplasm, and nucleus. Our experiments indicate that ROS significantly downregulates nuclear p-PPARγ and increases membrane AQP2 and αENaC; however, SR1664 (a nonagonist PPARγ ligand) reduces p-PPARγ and has no effect on AQP2 and αENaC. Therefore, we conclude that in vitro the fluid retention caused by ROS is associated with the increases in membrane αENaC and AQP2 but has little relevance to the phosphorylation of PPARγ. |
| format | Article |
| id | doaj-art-d15cc34f160b40d0be5cafe022e316f2 |
| institution | DOAJ |
| issn | 1687-4757 1687-4765 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | PPAR Research |
| spelling | doaj-art-d15cc34f160b40d0be5cafe022e316f22025-08-20T03:24:00ZengWileyPPAR Research1687-47571687-47652017-01-01201710.1155/2017/81309688130968Fluid Retention Caused by Rosiglitazone Is Related to Increases in AQP2 and αENaC Membrane ExpressionJinghua Xu0Mingyue Pan1Xiaoli Wang2Lishi Xu3Lanfang Li4Cheng Xu5Department of Physiology, School of Life Science and Biopharmaceutics, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenyang 110016, ChinaDepartment of Physiology, School of Life Science and Biopharmaceutics, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenyang 110016, ChinaDepartment of Physiology, School of Life Science and Biopharmaceutics, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenyang 110016, ChinaDepartment of Physiology, School of Life Science and Biopharmaceutics, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenyang 110016, ChinaDepartment of Physiology, School of Life Science and Biopharmaceutics, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenyang 110016, ChinaDepartment of Physiology, School of Life Science and Biopharmaceutics, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenyang 110016, ChinaPeroxisome proliferator activated receptor-γ (PPARγ) is a ligand-activated transcription factor of the nuclear hormone receptor superfamily. The decreased phosphorylation of PPARγ due to rosiglitazone (ROS) is the main reason for the increased insulin sensitivity caused by this antidiabetic drug. However, there is no clear evidence whether the nuclear translocation of p-PPARγ stimulated by ROS is related to fluid retention. It is also unclear whether the translocation of p-PPARγ is associated with the change of aquaporin-2 (AQP2) and epithelial sodium channel α subunit (αENaC) in membranes, cytoplasm, and nucleus. Our experiments indicate that ROS significantly downregulates nuclear p-PPARγ and increases membrane AQP2 and αENaC; however, SR1664 (a nonagonist PPARγ ligand) reduces p-PPARγ and has no effect on AQP2 and αENaC. Therefore, we conclude that in vitro the fluid retention caused by ROS is associated with the increases in membrane αENaC and AQP2 but has little relevance to the phosphorylation of PPARγ.http://dx.doi.org/10.1155/2017/8130968 |
| spellingShingle | Jinghua Xu Mingyue Pan Xiaoli Wang Lishi Xu Lanfang Li Cheng Xu Fluid Retention Caused by Rosiglitazone Is Related to Increases in AQP2 and αENaC Membrane Expression PPAR Research |
| title | Fluid Retention Caused by Rosiglitazone Is Related to Increases in AQP2 and αENaC Membrane Expression |
| title_full | Fluid Retention Caused by Rosiglitazone Is Related to Increases in AQP2 and αENaC Membrane Expression |
| title_fullStr | Fluid Retention Caused by Rosiglitazone Is Related to Increases in AQP2 and αENaC Membrane Expression |
| title_full_unstemmed | Fluid Retention Caused by Rosiglitazone Is Related to Increases in AQP2 and αENaC Membrane Expression |
| title_short | Fluid Retention Caused by Rosiglitazone Is Related to Increases in AQP2 and αENaC Membrane Expression |
| title_sort | fluid retention caused by rosiglitazone is related to increases in aqp2 and αenac membrane expression |
| url | http://dx.doi.org/10.1155/2017/8130968 |
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