| First Author | Qi H | Year | 2020 |
| Journal | Int Immunopharmacol | Volume | 88 |
| Pages | 106859 | PubMed ID | 32795896 |
| Mgi Jnum | J:345180 | Mgi Id | MGI:6821013 |
| Doi | 10.1016/j.intimp.2020.106859 | Citation | Qi H, et al. (2020) MicroRNA-16 directly binds to DEC2 and inactivates the TLR4 signaling pathway to inhibit lupus nephritis-induced kidney tissue hyperplasia and mesangial cell proliferation. Int Immunopharmacol 88:106859 |
| abstractText | Lupus nephritis (LN) is the most serious manifestation of systemic lupus erythematosus (SLE) and a major risk of mortality. This research focused on the function of microRNA-16 (miR-16) in LN development. Fcgamma receptor II-b-deficient (Fcgr2b(-/-)) mice with the natural potential to develop SLE- and LN-like diseases were used. Gain- and loss-of-function studies were performed to explore the function of miR-16 in pathological symptoms in mouse kidney tissues and the proliferation of mesangial cells (SV40 MES-13). The putative downstream molecules of miR-16 were explored. Consequently, poor expression of miR-16 was found in kidney tissues. Upregulation of miR-16 inhibited tissue hyperplasia, inflammatory infiltration, glomerular injury and fibrosis but increased cell apoptosis in mouse kidney tissues, and it inhibited proliferation but promoted apoptosis of MES-13 cells as well. miR-16 directly bound to DEC2 and inactivated the TLR4 signaling. DEC2 blocked the protective roles of miR-16 in MES-13 cells. The enhanced proliferation in MES-13 cells following miR-16 inhibition was reversed by chloroquine phosphate, a TLR4 antagonist. To sum up, miR-16 was evidenced to have a potent protective capacity in LN through relieving the LN symptoms in kidney tissues and reducing proliferation of mesangial cells, during which DEC2 silencing and TLR4 signaling deficit were involved. |
