Overexpression of circARF3 mitigates TNF-α-induced inflammatory damage by up-regulating miR-125b. Issue 11 (2nd June 2020)

• Record Type: Journal Article
• Authors: Zhang, Yingying; Hou, Binghui; Li, Chunxiao; Li, Hong
• Is Part Of: Cell cycle. Volume 19:Issue 11(2020)
• Page Start: 1253
• Page End: 1264
• Publication Date: 2020-06-02
• Subjects: Encephalitis -- TNF-α -- inflammation -- circARF3 -- miR-125b; Cell cycle -- Periodicals; 571.84377
• DOI: 10.1080/15384101.2020.1731652
• Languages: English
• ISSNs: 1538-4101

Abstract

ABSTRACT: Encephalitis is the highest disability illness. We studied the function and mechanisms of circular RNA circARF3 (circARF3) in neurocyte cell inflammatory damage. CCK-8 assay and flow cytometry were, respectively, employed for examining the influences of tumor necrosis factor α (TNF-α), circARF3 and microRNA (miR)-125b on cell viability and apoptosis. The expression of circARF3 and miR-125b were changed by employing cell transfection and the results were determined by using qRT-PCR. Besides, the expression of Bcl-2, Bax, Cleaved-caspase-3, interleukin (IL)-1β, IL-6, IL-8 and cell pathways-related proteins were examined by using Western blot. The productions of IL-6, IL-8 and IL-1β were also tested by ELISA. The level of reactive oxygen species (ROS) was examined by ROS assay. We found that TNF-α caused inflammatory damage showing as suppressed cell viability, enhanced cell apoptosis, and increased cytokines production and ROS generation. Besides, TNF-α inducement also markedly reduced circARF3 expression. circARF3 overexpression mitigated TNF-α-induced cell inflammatory damage. Moreover, miR-125b was targeted and positively regulated by circARF3. Furthermore, miR-125b inhibition could reverse the influences of circARF3 overexpression. Besides, circARF3 restrained the JNK and NF-κB pathways by up-regulation of miR-125b. In conclusion, overexpression of circARF3 mitigated cell inflammatory damage via inactivation of JNK and NF-κB pathways and thereby up-regulation of miR-125b.