Down-regulated circ_0001853 inhibits lipopolysaccharide-induced endometritis progression via sponging miR-34c-5p

IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS
Qian Xu, Ailing Peng, Liyun Zhao, Li Wang
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引用次数: 0

Abstract

Background

To investigate the diagnostic value and mechanism of action of circular RNA (circ_) circ_0001853 and microRNA (miR) miR-34c-5p in patients with endometritis.

Methods

189 patients with endometritis and 176 healthy individuals were included in this study. Venous blood serum was collected from the study subjects and stored temporarily at −80 °C. Real-time quantitative chain polymerase reaction (RT-qPCR) was used to detect circ_0001853 and miR-34c-5p expression, and receiver operating characteristic (ROC) curves assessed the diagnostic value of both in predicting endometritis. Cell counting kit (CCK8) observed cell proliferation, flow cytometry recorded apoptosis, enzyme linked immunosorbent assay (ELISA) monitored inflammatory factor expression, and dual luciferase reporter assay and RNA immunoprecipitation (RIP) verified the relationship between circ_0001853 and miR-34c-5p targeting interactions.

Results

High levels of circ_0001853 and low levels of miR-34c-5p were present in endometritis patients, and they were negatively correlated. Both circ_0001853 and miR-34c-5p alone or in combination had diagnostic value in predicting the progression of endometritis. Transfection of si-circ_0001853 promoted cell proliferation and reduced apoptosis and cellular inflammation levels induced by lipopolysaccharide (LPS) stimulation. There was a direct reciprocal targeting relationship between miR-34c-5p and circ_0001853, and the use of miR-34c-5p inhibitor resisted silencing circ_0001853 promoted cell proliferation and increased the number of apoptotic cells and cellular inflammation levels.

Conclusions

circ_0001853 is involved in endometritis progression through miR-34c-5p, i.e., low circ_0001853 promotes miR-34c-5p-induced proliferation of epithelial cells, reduces apoptosis, and suppresses inflammation levels, preventing disease progression.
下调的circ_0001853通过海绵miR-34c-5p抑制脂多糖诱导的子宫内膜炎进展。
背景:探讨环状RNA (circ_) circ_0001853和microRNA (miR) miR-34c-5p在子宫内膜炎患者中的诊断价值及作用机制。方法:189例子宫内膜炎患者和176名健康人作为研究对象。采集研究对象静脉血血清,在-80°C临时保存。采用实时定量链聚合酶反应(RT-qPCR)检测circ_0001853和miR-34c-5p的表达,并用受试者工作特征(ROC)曲线评估两者在预测子宫内膜炎中的诊断价值。细胞计数试剂盒(CCK8)观察细胞增殖,流式细胞术记录细胞凋亡,酶联免疫吸附试验(ELISA)监测炎症因子表达,双荧光素酶报告基因法和RNA免疫沉淀(RIP)验证circ_0001853与miR-34c-5p靶向相互作用之间的关系。结果:子宫内膜炎患者存在高水平的circ_0001853和低水平的miR-34c-5p,两者呈负相关。circ_0001853和miR-34c-5p单独或联合使用对预测子宫内膜炎的进展具有诊断价值。转染si-circ_0001853可促进细胞增殖,减少脂多糖(LPS)刺激引起的细胞凋亡和细胞炎症水平。miR-34c-5p与circ_0001853之间存在直接的相互靶向关系,使用miR-34c-5p抑制剂抵抗circ_0001853的沉默,促进细胞增殖,增加凋亡细胞数量和细胞炎症水平。结论:circ_0001853通过miR-34c-5p参与子宫内膜炎的进展,即低circ_0001853促进miR-34c-5p诱导的上皮细胞增殖,减少凋亡,抑制炎症水平,防止疾病进展。
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来源期刊
Molecular and Cellular Probes
Molecular and Cellular Probes 生物-生化研究方法
CiteScore
6.80
自引率
0.00%
发文量
52
审稿时长
16 days
期刊介绍: MCP - Advancing biology through–omics and bioinformatic technologies wants to capture outcomes from the current revolution in molecular technologies and sciences. The journal has broadened its scope and embraces any high quality research papers, reviews and opinions in areas including, but not limited to, molecular biology, cell biology, biochemistry, immunology, physiology, epidemiology, ecology, virology, microbiology, parasitology, genetics, evolutionary biology, genomics (including metagenomics), bioinformatics, proteomics, metabolomics, glycomics, and lipidomics. Submissions with a technology-driven focus on understanding normal biological or disease processes as well as conceptual advances and paradigm shifts are particularly encouraged. The Editors welcome fundamental or applied research areas; pre-submission enquiries about advanced draft manuscripts are welcomed. Top quality research and manuscripts will be fast-tracked.
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