CircDCLRE1C Regulated Lipopolysaccharide-Induced Inflammatory Response and Apoptosis by Regulating miR-214b-3p/STAT3 Pathway in Macrophages
文献类型： 外文期刊
作者： Xu, Yibin 1 ; Huang, Yulin 1 ; Zhang, Siyu 1 ; Guo, Lijin 1 ; Wu, Ruiquan 1 ; Fang, Xiang 1 ; Chen, Xiaolan 6 ; Xu, Haiping 1 ; Nie, Qinghua 1 ;
作者机构： 1.South China Agr Univ, Coll Anim Sci, Dept Anim Genet Breeding & Reprod, Guangzhou 510642, Peoples R China
2.Minist Agr, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Guangzhou 510642, Peoples R China
3.Minist Agr, Key Lab Chicken Genet Breeding & Reprod, Guangzhou 510642, Peoples R China
4.South China Agr Univ, Coll Anim Sci, State Key Lab Conservat & Utilizat Subtrop Agrobi, Guangzhou 510642, Peoples R China
5.South China Agr Univ, Coll Anim Sci, Lingnan Guangdong Lab Agr, Guangzhou 510642, Peoples R China
6.Chongqing Univ, Sch Life Sci, Chongqing 401331, Peoples R China
关键词： circular RNA; inflammation; apoptosis; miR-214b-3p; STAT3; macrophage
期刊名称：INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES （ 影响因子：6.208； 五年影响因子：6.628 ）
ISSN：
年卷期： 2022 年 23 卷 12 期
页码：
收录情况： SCI
摘要： The immune cell inflammation response is closely related to the occurrence of disease, and much evidence has shown that circular RNAs (circRNAs) play vital roles in the occurrence of disease. However, the biological function and regulatory mechanisms of circRNAs in the immune cell inflammation response remain poorly understood. In this study, we constructed an inflammatory model using lipopolysaccharide (LPS)-stimulated chicken macrophage lines (also known as HD11) to verify the function and mechanism of the novel circDCLRE1C (ID: gga_circ_0001674), which was significantly upregulated in spleen tissues infected by coccidia and the macrophage cells exposed to LPS. The results showed that circDCLRE1C aggravated LPS-induced inflammation and apoptosis in HD11 cells. Systemically, circDCLRE1C acted as a sponge for miR-214b-3p binding sites thereby regulating the expression of STAT3. The overexpression of miR-214b-3p rescued the pro-inflammatory effect of circDCLRE1C in HD11 cells stimulated with LPS, and rescued the high expression of STAT3. In conclusion, our study showed that circDCLRE1C could aggravate LPS-induced inflammation and apoptosis through competitive adsorption of miR-214b-3p, thereby increasing the expression of STAT3.
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