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Retracted : Silencing circular RNA circANKRD36 remits lipopolysaccharide‐induced inflammatory damage by regulating microRNA‐15/MyD88
Author(s) -
Wang Qiaoyan,
Tao Shujun,
Zhu Nan,
Li Tingting,
Yu Lingling
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29490
Subject(s) - hacat , viability assay , gene silencing , chemistry , transfection , flow cytometry , apoptosis , lipopolysaccharide , microbiology and biotechnology , microrna , small interfering rna , cell , biology , immunology , in vitro , biochemistry , gene
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)‐1β, IL‐6, and proteins of the pathway were investigated by Western blot. Otherwise, the levels of IL‐1β 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‐κB 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‐κB pathway in HaCaT cells.