Inhibition of miR-17~92 Cluster Ameliorates High Glucose-Induced Podocyte Damage
The loss and damage of podocytes is an early feature of diabetic nephropathy (DN). The miR-17∼92 cluster was dysregulated in diabetic and polycystic kidney disease patients, but its role in DN is unclear. Hence, an in vitro study on the high glucose- (HG-) treated mouse podocytes (MPC5) was designed...
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| Format: | Article |
| Language: | English |
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Wiley
2020-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2020/6126490 |
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| author | Xiaobao Fan Zhiming Hao Zhenjiang Li Xiaoming Wang Jing Wang |
| author_facet | Xiaobao Fan Zhiming Hao Zhenjiang Li Xiaoming Wang Jing Wang |
| author_sort | Xiaobao Fan |
| collection | DOAJ |
| description | The loss and damage of podocytes is an early feature of diabetic nephropathy (DN). The miR-17∼92 cluster was dysregulated in diabetic and polycystic kidney disease patients, but its role in DN is unclear. Hence, an in vitro study on the high glucose- (HG-) treated mouse podocytes (MPC5) was designed to elucidate the effect of miR-17∼92 cluster downregulation on cell viability, apoptosis, inflammation, fibrosis, and podocyte function. The results suggested that the miR-17∼92 cluster members miR-17-5p, miR-18a, miR-19a, miR-19b, miR-20a, and miR-92a were upregulated in the renal biopsy tissue of DN patients and HG-treated MPC5. The downregulation of the miR-17∼92 cluster effectively suppressed the cell apoptosis, inflammation, fibrosis, and podocyte dysfunction in HG-stimulated MPC5 cells. The bioinformatics analysis and rescue experiments showed that ABCA1 (ATP-binding cassette transporter A1) is an effector of the miR-17~92 cluster. Silence of ABCA1 inhibited the protective effect of the miR-17∼92 cluster downregulation on podocyte damage. In summary, this research indicated that the downregulation of the miR-17∼92 cluster ameliorates HG-induced podocyte damage via targeting ABCA1. |
| format | Article |
| id | doaj-art-264b152f6453482eb499b76564cdefe7 |
| institution | OA Journals |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2020-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-264b152f6453482eb499b76564cdefe72025-08-20T02:04:26ZengWileyMediators of Inflammation0962-93511466-18612020-01-01202010.1155/2020/61264906126490Inhibition of miR-17~92 Cluster Ameliorates High Glucose-Induced Podocyte DamageXiaobao Fan0Zhiming Hao1Zhenjiang Li2Xiaoming Wang3Jing Wang4Department of Rheumatology and Immunology, The First Affiliated Hospital of Medical College of Xi’an Jiaotong University, Xi’an City, Shaanxi Province 710061, ChinaDepartment of Rheumatology and Immunology, The First Affiliated Hospital of Medical College of Xi’an Jiaotong University, Xi’an City, Shaanxi Province 710061, ChinaNephrotic Hemodialysis Center, Shaanxi Provincial People’s Hospital, Xi’an City, Shaanxi Province 710068, ChinaNephrotic Hemodialysis Center, Shaanxi Provincial People’s Hospital, Xi’an City, Shaanxi Province 710068, ChinaNephrotic Hemodialysis Center, Shaanxi Provincial People’s Hospital, Xi’an City, Shaanxi Province 710068, ChinaThe loss and damage of podocytes is an early feature of diabetic nephropathy (DN). The miR-17∼92 cluster was dysregulated in diabetic and polycystic kidney disease patients, but its role in DN is unclear. Hence, an in vitro study on the high glucose- (HG-) treated mouse podocytes (MPC5) was designed to elucidate the effect of miR-17∼92 cluster downregulation on cell viability, apoptosis, inflammation, fibrosis, and podocyte function. The results suggested that the miR-17∼92 cluster members miR-17-5p, miR-18a, miR-19a, miR-19b, miR-20a, and miR-92a were upregulated in the renal biopsy tissue of DN patients and HG-treated MPC5. The downregulation of the miR-17∼92 cluster effectively suppressed the cell apoptosis, inflammation, fibrosis, and podocyte dysfunction in HG-stimulated MPC5 cells. The bioinformatics analysis and rescue experiments showed that ABCA1 (ATP-binding cassette transporter A1) is an effector of the miR-17~92 cluster. Silence of ABCA1 inhibited the protective effect of the miR-17∼92 cluster downregulation on podocyte damage. In summary, this research indicated that the downregulation of the miR-17∼92 cluster ameliorates HG-induced podocyte damage via targeting ABCA1.http://dx.doi.org/10.1155/2020/6126490 |
| spellingShingle | Xiaobao Fan Zhiming Hao Zhenjiang Li Xiaoming Wang Jing Wang Inhibition of miR-17~92 Cluster Ameliorates High Glucose-Induced Podocyte Damage Mediators of Inflammation |
| title | Inhibition of miR-17~92 Cluster Ameliorates High Glucose-Induced Podocyte Damage |
| title_full | Inhibition of miR-17~92 Cluster Ameliorates High Glucose-Induced Podocyte Damage |
| title_fullStr | Inhibition of miR-17~92 Cluster Ameliorates High Glucose-Induced Podocyte Damage |
| title_full_unstemmed | Inhibition of miR-17~92 Cluster Ameliorates High Glucose-Induced Podocyte Damage |
| title_short | Inhibition of miR-17~92 Cluster Ameliorates High Glucose-Induced Podocyte Damage |
| title_sort | inhibition of mir 17 92 cluster ameliorates high glucose induced podocyte damage |
| url | http://dx.doi.org/10.1155/2020/6126490 |
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