MicroRNA-18a-5p mitigates oxygen-glucose-deprivation/reoxygenation-induced injury through suppression of TLRs/NF-κB signaling by targeting TLR8 in PC12 cells

被引:9
作者
Lu, Ying-Yun [1 ]
Ma, Xiao-Jun [2 ]
Yang, Yan-Na [3 ]
机构
[1] Shandong Prov Third Hosp, Dept Severe Rehabil, Jinan, Peoples R China
[2] Shandong Prov Third Hosp, Dept Geriatr, Jinan, Peoples R China
[3] Shandong First Med Univ, Dept Resp, Jinan Cent Hosp, Jinan, Peoples R China
关键词
OGD/R; miR-18a-5p; TLR8; TLRs; NF-kappa B; ISCHEMIA-REPERFUSION INJURY; TOLL-LIKE RECEPTORS; ISCHEMIA/REPERFUSION INJURY; STROKE; PATHWAY; EXPRESSION; MIR-18A-5P; CANCER;
D O I
10.1080/09168451.2020.1806705
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 work aimed to assess the role of TLR8 in cerebral I/R injury and its in-depth pathogenesis. Bioinformatics analysis indicated that TLR8 was up-regulated in patients with ischemic stroke than that in healthy control, and miR-18a-5p was the upstream regulatory of TLR8. Then, the rat pheochromocytoma PC12 cells were exposed in oxygen-glucose-deprivation/reoxygenation (OGD/R) conditions to construct a modelin vitro. The functional experiments indicated that OGD/R can decline the viability and elevate the apoptosis of PC12 cells, while up-regulation of miR-18a-5p can alleviate OGD/R-induced cell injury. Notably, overexpression of TLR8 reverses the miR-18a-5p-mediated protection on OGD/R-induced cells injury. Finally, we found that up-regulation of miR-18a-5p obviously declined the protein levels of TLR4 and TLR7 as well as the phosphorylation of NF-kappa B, while overexpression of TLR8 canceled the decrease caused by miR-18a-5p up-regulation. In summing, our results illustrated that miR-18a-5p/TLR8 axis can mitigate OGD/R-induced cells injury through TLRs and NF-kappa B pathway.
引用
收藏
页码:2476 / 2483
页数:8
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