| First Author | Sun W | Year | 2017 |
| Journal | FEBS Lett | Volume | 591 |
| Issue | 21 | Pages | 3588-3599 |
| PubMed ID | 28976551 | Mgi Jnum | J:258328 |
| Mgi Id | MGI:6117931 | Doi | 10.1002/1873-3468.12872 |
| Citation | Sun W, et al. (2017) miR-181c protects CsA-induced renal damage and fibrosis through inhibiting EMT. FEBS Lett 591(21):3588-3599 |
| abstractText | Cyclosporine A (CsA), a widely used immunosuppressive drug in organ transplantation and autoimmune disorders, frequently induces renal damage and fibrosis. Recent evidence has implicated epithelial-mesenchymal transition (EMT) in CsA-induced nephrotoxicity. Microarray analysis disclosed miR-181c as the microRNA most dramatically repressed by CsA. Downregulation of miR-181c expression at the transcriptional level by CsA is dependent on the transcription factor Nrf2. miR-181c mimics or inhibitors attenuate or aggravate CsA-induced EMT gene changes, respectively. Importantly, in Nrf2-/- mice, CsA-induced renal damage, fibrosis, and EMT gene changes are restored by miR-181c mimics. Mechanistically, we identified Notch2 as a potential target of miR-181c. Collectively, our data support the notion that miR-181c may serve as an important factor for protecting renal tissues from CsA-induced nephrotoxicity. |
