Department of Pediatrics, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, HuBei 430072, China.
College of Life Sciences, Wuhan University, Wuhan 430072, China.
Biomed Res Int. 2021 Jan 6;2021:7413605. doi: 10.1155/2021/7413605. eCollection 2021.
Inflammation is an important biological process for eliciting immune responses against physiological and pathological stimuli. Inflammation must be efficiently regulated to ensure homeostasis in the body. Nuclear factor-kappa B (NF-B) signaling is crucial for inflammatory and immune responses. Aberrant activation of NF-B signaling leads to development of numerous human diseases. In this study, we investigated the function of chromosome 7 open reading frame 41 (C7ORF41) in NF-B signaling during inflammation. C7ORF41 was upregulated in cells stimulated with tumor necrosis factor-alpha or lipopolysaccharide. Moreover, overexpression of C7ORF41 inhibited the activation of NF-B and decreased the expression of its downstream target genes. Notably, small hairpin RNA-mediated depletion of C7ORF41 increased the levels of downstream genes and enabled the activation of NF-B. In conclusion, C7ORF41 negatively regulated inflammation via NF-B signaling and p65 phosphorylation . These findings may help to diagnose and prognosticate inflammatory conditions and may help develop new strategies for the management of inflammation-related diseases.
炎症反应是机体针对生理和病理刺激产生免疫应答的一种重要生物学过程。炎症反应必须得到有效调控,以确保机体内环境的稳定。核因子-κB(NF-κB)信号通路对于炎症和免疫反应至关重要。NF-κB 信号通路的异常激活可导致多种人类疾病的发生。在本研究中,我们探讨了染色体 7 开放阅读框 41(C7ORF41)在炎症反应过程中对 NF-κB 信号通路的作用。在受到肿瘤坏死因子-α或脂多糖刺激的细胞中,C7ORF41 的表达上调。此外,过表达 C7ORF41 可抑制 NF-κB 的激活,并降低其下游靶基因的表达。值得注意的是,利用小发夹 RNA 敲低 C7ORF41 的表达可增加下游基因的水平,从而激活 NF-κB。综上所述,C7ORF41 通过 NF-κB 信号通路和 p65 磷酸化负向调控炎症反应。这些发现可能有助于炎症状态的诊断和预后,并可能有助于开发针对炎症相关疾病的新治疗策略。