期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 88, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.intimp.2020.106859
关键词
MicroRNA-16; DEC2; TLR4 signaling pathway; Systemic lupus erythematosus; Lupus nephritis; Hyperplasia
资金
- Chinese National Natural Science Fundation for Young Scientists [81900642]
- Scientific Research Fundation for Seeding Project of Young Scientific and Technological Talents of Liaoning Provincial Education Department [QN2019006]
- Youth Backbone Foundation of China Medical University [1210519033]
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.
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