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RETRACTED: Silencing circular RNA circANKRD36 remits lipopolysaccharide-induced inflammatory damage by regulating microRNA-15/MyD88 (Retracted Article)
被引:3
|作者:
Wang, Qiaoyan
[1
]
Tao, Shujun
[1
]
Zhu, Nan
[1
]
Li, Tingting
[1
]
Yu, Lingling
[2
]
机构:
[1] Qingdao 6 Peoples Hosp, Dept Hepatopathy 2, Qingdao, Shandong, Peoples R China
[2] Qingdao 6 Peoples Hosp, Dept Hepatopathy 10, 9 Fushun Rd, Qingdao 266033, Shandong, Peoples R China
关键词:
bedsore;
circANKRD36;
inflammatory damage;
LPS;
miR-15;
MIR-15/16;
PROLIFERATION;
EXPRESSION;
TARGETS;
PATHWAY;
CANCER;
D O I:
10.1002/jcb.29490
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:
Bedsore is a familiar disease, which fearfully harms the health of the patients. We investigated the efficacy and mechanism of circular RNA circANKRD36 on HaCaT cell in inflammatory damage. CCK-8 and flow cytometry were respectively used to investigate the efficacies of lipopolysaccharide (LPS), circANKRD36, and microRNA (miR)-15 on cell viability and apoptosis. Moreover, circANKRD36 and miR-15 expression were changed by cell transfection and investigated by reverse transcription-quantitative polymerase chain reaction. Furthermore, the levels of Bax, pro caspase-3, cleaved caspase-3, interleukin (IL)-1 beta, IL-6, and proteins of the pathway were investigated by Western blot. Otherwise, the levels of IL-1 beta and IL-6 were investigated by enzyme-linked immunosorbent assay. Reactive oxygen species (ROS) was investigated by ROS assay. The relation between myeloid differentiation factor 88 (MyD88) and miR-15 was investigated by luciferase assay. LPS caused inflammatory damage and upregulated circANKRD36. circANKRD36 was silenced in cells and si-circANKRD36 remitted inflammatory damage. Furthermore, si-circANKRD36 negatively regulated miR-15 and miR-15 inhibitor could reverse the efficacies of si-circANKRD36. Besides, si-circANKRD36 restrained the NF-kappa B pathway by upregulating miR-15. Finally, MyD88 was authenticated as a target of miR-15. circANKRD36 remitted cell inflammatory damage upregulating miR-15/MyD88 via the NF-kappa B pathway in HaCaT cells.
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页码:2704 / 2712
页数:9
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