MicroRNA-223 inhibits lipopolysaccharide-induced inflammatory response by directly targeting Irak1 in the nucleus pulposus cells of intervertebral disc

被引:41
作者
Wang, Hua [1 ]
Hao, Pan [2 ]
Zhang, Hu [3 ]
Xu, Cuiping [1 ]
Zhao, Junyan [1 ]
机构
[1] Shandong Prov Qianfoshan Hosp, Dept Orthoped, 16766 Jingshi Rd, Jinan 250014, Shandong, Peoples R China
[2] Jinan Cent Hosp, Dept Spinal & Joint Surg, Jinan, Shandong, Peoples R China
[3] Shandong Prov Qianfoshan Hosp, Dept Nursing, Jinan, Shandong, Peoples R China
关键词
intervertebral disc degeneration; Irak1; inflammation; lipopolysaccharide; miR-223; PROLIFERATION; EXPRESSION; DEGENERATION; MEDIATORS; MECHANISM; APOPTOSIS; GENOMICS; GROWTH;
D O I
10.1002/iub.1747
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
This study was aimed to research the effect of miR-223 on the inflammatory responses induced by lipopolysaccharide (LPS) in nucleus pulposus (NP) cells of rat intervertebral disc. Isolated rat NP cells were induced by LPS. Reverse transcriptase quantitative real-time polymerase chain reaction was used to detect gene expression. To detect protein expression, Western blot and enzyme-linked immunosorbent assay experiments were applied. The putative targeting relationship between miR-223 and Irak1 was determined using dual-luciferase reporter gene assay. We found that miR-223 was downregulated in LPS-induced NP cells. MiR-223 upregulated the expression of extracellular matrix-related genes (Aggrecan and Collagen II). Matrix degrading enzymes (ADAMTS4, ADAMTS5, MMP3 and MMP13), NO reaction-associated proteins (PGE2, COX-2 and INOS) and the expression of nuclear factor (NF)-B signaling-related proteins were downregulated after miR-233 overexpression. In addition, luciferase reporter assays demonstrated that miR-223 directly targeted Irak1. MiR-223 overexpression could inhibit NF-B signaling by targeting Irak1, and finally suppress the LPS-induced inflammation in NP cells. (c) 2018 IUBMB Life, 70(6):479-490, 2018
引用
收藏
页码:479 / 490
页数:12
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