MicroRNA-10 negatively regulates inflammation in diabetic kidney via targeting activation of the NLRP3 inflammasome

• DOI: 10.1016/j.ymthe.2021.03.012
• Publication Date: 2021-03-18T19:15:09Z
• Authors: Hanying Ding; Jinxiang Li; Yang Li; Minliang Yang; Sheng Nie; Miaomiao Zhou; Zhanmei Zhou; Xiaobing Yang; Youhua Liu; Fan Fan Hou
• Keywords: Pyrin domain; Albuminuria; Mediator

NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3) inflammasome activation has emerged as a central mediator of kidney inflammation in diabetic disease (DKD). However, the mechanism underlying this DKD remains poorly defined. In study, we found that kidney-enriched microRNA-10a -10b (miR-10a/b), predominantly expressed podocytes tubular epithelial cells, were downregulated from mice patients with DKD. High glucose decreased miR-10a/b expression vitro an osmolarity-independent manner. functioned negative regulators through targeting 3′untranslated region mRNA, inhibiting assembly decreasing caspase-1-dependent release pro-inflammatory cytokines. Delivery into prevented renal inflammation, it reduced albuminuria streptozotocin (STZ)-treated mice, whereas knocking down increased activation. Restoration established ameliorated mitigated both db/db STZ-treated mice. These results suggest novel intervention strategy for by inflammasome.