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CircPRKCI relieves lipopolysaccharide-induced HK2 cell injury by upregulating the expression of miR-545 target gene ZEB2.
Biofactors ( IF 6 ) Pub Date : 2020-02-27 , DOI: 10.1002/biof.1620
Xiaofeng Shi 1 , Wei Ma 2 , Yongqi Li 3 , Han Wang 4 , Shuang Pan 5 , Yongquan Pan 6 , Caiming Xu 7 , Lei Li 6
Affiliation  

The aim of this study was to investigate the possible influences of circPRKCI abnormal expression on lipopolysaccharide (LPS)‐induced HK2 cell injury and its mechanism. The circPRKCI level was identified in serum samples from patients with urosepsis and healthy subjects, as well as LPS‐treated HK2 cells by qRT‐PCR. Cell viability, apoptosis, expression of proteins associated with apoptosis, and expression of pro‐inflammatory cytokines in LPS‐treated HK2 cells were measured. Effects of circPRKCI abnormal expression on LPS‐induced HK2 cell injury were then evaluated. Afterward, the binding miRNA of circPRKCI and target gene of miRNA were identified, and the involvements of NF‐kB pathway signaling pathway with the effects of circPRKCI were finally studied. CircPRKCI was significantly down‐regulated in serum samples from patients with urosepsis and LPS‐treated HK2 cells. LPS‐induced decrease of cell viability, increase of cell apoptosis, as well as elevated productions of tumor necrosis factor (TNF)‐α, interleukins (IL)‐1β, IL‐6, and IL‐8 in HK2 cells were attenuated by overexpressed circPRKCI. In addition, circPRKCI negatively regulated the expression of miR‐545, and miR‐545 up‐regulation reversed the inhibiting effects of circPRKCI overexpression on LPS‐induced HK2 cell injury. Moreover, zinc finger E‐box‐binding homeobox 2 (ZEB2) was identified as a target gene of miR‐545, and ZEB2 overexpression partly reversed the effects of miR‐545 up‐regulation on LPS‐induced HK2 cell injury. Furthermore, NF‐kB pathway was revealed to be associated to the effects of circPRKCI on LPS‐induced HK2 cell injury. This research indicated that the highly expressed circPRKCI relieved inflammatory injury induced by LPS in HK2 cells by suppressing miR‐545/ZEBs and depressing the briskness of NF‐kB pathway.

中文翻译:

CircPRKCI通过上调miR-545目标基因ZEB2的表达来减轻脂多糖诱导的HK2细胞损伤。

这项研究的目的是研究circPRKCI异常表达对脂多糖(LPS)诱导的HK2细胞损伤的可能影响及其机制。通过qRT-PCR在尿毒症患者和健康受试者的血清样本以及经LPS处理的HK2细胞中鉴定出circPRKCI水平。测量了LPS处理的HK2细胞的细胞活力,凋亡,与凋亡相关的蛋白的表达以及促炎细胞因子的表达。然后评估circPRKCI异常表达对LPS诱导的HK2细胞损伤的影响。随后,鉴定了circPRKCI的miRNA与miRNA的靶基因的结合,最终研究了NF-kB途径信号通路与circPRKCI作用的关系。在尿检和LPS处理的HK2细胞患者的血清样本中,CircPRKCI显着下调。LPS诱导的HK2细胞过度表达减弱了LPS诱导的细胞活力降低,细胞凋亡增加以及肿瘤坏死因子(TNF)-α,白介素(IL)-1β,IL-6和IL-8产生的增加circPRKCI。此外,circPRKCI负调节miR-545的表达,而miR-545上调逆转了circPRKCI过表达对LPS诱导的HK2细胞损伤的抑制作用。此外,锌指结合E-box的同源盒2(ZEB2)被确定为miR-545的靶基因,而ZEB2的过表达部分逆转了miR-545上调对LPS诱导的HK2细胞损伤的作用。此外,发现NF-kB通路与circPRKCI对LPS诱导的HK2细胞损伤的影响有关。
更新日期:2020-02-27
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