BKCa Mediates Dysfunction in High Glucose Induced Mesangial Cell Injury via TGF-β1/Smad2/3 Signaling Pathways
Objective. To explore the role and mechanism of BKCa in diabetic kidney disease. Methods. Rat mesangial cells (MCs) HBZY-1 were cultured with high glucose to simulate the high-glucose environment of diabetic kidney disease in vivo. The effects of large conductance calcium-activated potassium channel...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2020-01-01
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| Series: | International Journal of Endocrinology |
| Online Access: | http://dx.doi.org/10.1155/2020/3260728 |
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| author | Zhigui Wu Wenxian Yin Mengqi Sun Yuankai Si Xiaoxiao Wu Meijuan Chen |
| author_facet | Zhigui Wu Wenxian Yin Mengqi Sun Yuankai Si Xiaoxiao Wu Meijuan Chen |
| author_sort | Zhigui Wu |
| collection | DOAJ |
| description | Objective. To explore the role and mechanism of BKCa in diabetic kidney disease. Methods. Rat mesangial cells (MCs) HBZY-1 were cultured with high glucose to simulate the high-glucose environment of diabetic kidney disease in vivo. The effects of large conductance calcium-activated potassium channel (BKCa) on proliferation, migration, and apoptosis of HBZY-1 cells were observed. The contents of transforming growth factor beta 1 (TGF-β1), Smad2/3, collagen IV (Col IV), and fibronectin (FN) in the extracellular matrix were also observed. Results. High glucose significantly damaged HBZY-1 cells, which enhanced the ability of cell proliferation, migration, and apoptosis, and increased the secretion of Col IV and FN. Inhibition of BKCa and TGF-β1/Smad2/3 signaling pathways can inhibit the proliferation, migration, and apoptosis of HBZY-1 cells and suppress the secretion of Col IV and FN. The effect of excitation is the opposite. Conclusions. BKCa regulates mesangial cell proliferation, migration, apoptosis, and secretion of Col IV and FN and is associated with TGF-β1/Smad2/3 signaling pathway. |
| format | Article |
| id | doaj-art-c6e7a93d75314cb1957b92ea13886ee5 |
| institution | DOAJ |
| issn | 1687-8337 1687-8345 |
| language | English |
| publishDate | 2020-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Endocrinology |
| spelling | doaj-art-c6e7a93d75314cb1957b92ea13886ee52025-08-20T03:23:34ZengWileyInternational Journal of Endocrinology1687-83371687-83452020-01-01202010.1155/2020/32607283260728BKCa Mediates Dysfunction in High Glucose Induced Mesangial Cell Injury via TGF-β1/Smad2/3 Signaling PathwaysZhigui Wu0Wenxian Yin1Mengqi Sun2Yuankai Si3Xiaoxiao Wu4Meijuan Chen5Department of Pharmacy, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, ChinaDepartment of Pharmacy, Affiliated Hospital of Traditional Chinese Medicine Southwest Medical University, Luzhou 646000, Sichuan, ChinaDepartment of Pharmacy, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, ChinaDepartment of Pharmacy, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, ChinaDepartment of Pharmacy, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, ChinaDepartment of Pharmacy, Southwest Medical University, Luzhou 646000, Sichuan, ChinaObjective. To explore the role and mechanism of BKCa in diabetic kidney disease. Methods. Rat mesangial cells (MCs) HBZY-1 were cultured with high glucose to simulate the high-glucose environment of diabetic kidney disease in vivo. The effects of large conductance calcium-activated potassium channel (BKCa) on proliferation, migration, and apoptosis of HBZY-1 cells were observed. The contents of transforming growth factor beta 1 (TGF-β1), Smad2/3, collagen IV (Col IV), and fibronectin (FN) in the extracellular matrix were also observed. Results. High glucose significantly damaged HBZY-1 cells, which enhanced the ability of cell proliferation, migration, and apoptosis, and increased the secretion of Col IV and FN. Inhibition of BKCa and TGF-β1/Smad2/3 signaling pathways can inhibit the proliferation, migration, and apoptosis of HBZY-1 cells and suppress the secretion of Col IV and FN. The effect of excitation is the opposite. Conclusions. BKCa regulates mesangial cell proliferation, migration, apoptosis, and secretion of Col IV and FN and is associated with TGF-β1/Smad2/3 signaling pathway.http://dx.doi.org/10.1155/2020/3260728 |
| spellingShingle | Zhigui Wu Wenxian Yin Mengqi Sun Yuankai Si Xiaoxiao Wu Meijuan Chen BKCa Mediates Dysfunction in High Glucose Induced Mesangial Cell Injury via TGF-β1/Smad2/3 Signaling Pathways International Journal of Endocrinology |
| title | BKCa Mediates Dysfunction in High Glucose Induced Mesangial Cell Injury via TGF-β1/Smad2/3 Signaling Pathways |
| title_full | BKCa Mediates Dysfunction in High Glucose Induced Mesangial Cell Injury via TGF-β1/Smad2/3 Signaling Pathways |
| title_fullStr | BKCa Mediates Dysfunction in High Glucose Induced Mesangial Cell Injury via TGF-β1/Smad2/3 Signaling Pathways |
| title_full_unstemmed | BKCa Mediates Dysfunction in High Glucose Induced Mesangial Cell Injury via TGF-β1/Smad2/3 Signaling Pathways |
| title_short | BKCa Mediates Dysfunction in High Glucose Induced Mesangial Cell Injury via TGF-β1/Smad2/3 Signaling Pathways |
| title_sort | bkca mediates dysfunction in high glucose induced mesangial cell injury via tgf β1 smad2 3 signaling pathways |
| url | http://dx.doi.org/10.1155/2020/3260728 |
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