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Abstract：
UNASSIGNED: This study sought to explore the role and molecular mechanism of circ_0049271 in hypoxia-reoxygenation (H/R)-induced cardiomyocyte injury.
UNASSIGNED: Significantly upregulated circular ribonucleic acids (circRNAs) in Gene Expression Omnibus (GEO) data sets were identified using a Venn diagram. A H9c2 (rat cardiomyocytes) cell model of acute myocardial infarction (AMI) was induced by 1% H/R. Quantitative reverse transcription-polymerase chain reaction was used to detect the expression levels of circ_0049271, miR-17-3p, and FZD4 in clinical blood samples and cells, and Cell Counting Kit-8 (CCK-8) was used to determine the proliferation rate of the cells in each group. Next, flow cytometry and Western blot were used to evaluate cell apoptosis. Biochemical tests and enzyme-linked immunosorbent assays (ELISAs) were then used to determine the activities/levels of the cell damage markers [i.e., creatine kinase (CK) and lactate dehydrogenase (LDH)], oxidative stress substances [i.e., malondialdehyde (MDA), reactive oxygen species (ROS), and superoxide dismutase (SOD)], and inflammatory factors [i.e., interleukin (IL)-1β, IL-6, and IL-8]. In addition, intermolecular interactions were verified using dual-luciferase reporter and RNA pull-down experiments.
UNASSIGNED: Circ_0049271 was significantly upregulated in both the blood of the AMI patients and the H/R-induced H9c2 cells. The knockdown of circ_0049271 increased the cell proliferation rate, decreased the apoptosis rate, inhibited oxidative stress (ROS and MDA were upregulated, and SOD was downregulated) and inflammatory responses (IL-1, IL-6, and IL-8 were downregulated), and relieved cell damage. However, the overexpression of circ_0049271 promoted H/R-induced H9c2 cell damage. Further experiments showed that miR-17-3p was a target of circ_0049271, and miR-17-3p was negatively correlated with circ_0049271 in the AMI blood samples. Additionally, miR-17-3p was found to target FZD4. A further exploration also revealed that miR-17-3p knockdown or FZD4 overexpression reversed the effects of si-circ_0049271 on the H/R-induced H9c2 cells; that is, miR-17-3p knockdown or FZD4 overexpression promoted H/R-induced injury in the H9c2 cells.
UNASSIGNED: Circ_0049271 promoted cellular function damage (e.g., proliferation inhibition, apoptosis, oxidative stress, and inflammation) in H/R-induced H9c2 cardiomyocytes via the miR-17-3p/FZD4 signaling axis.
UNASSIGNED: Significantly upregulated circular ribonucleic acids (circRNAs) in Gene Expression Omnibus (GEO) data sets were identified using a Venn diagram. A H9c2 (rat cardiomyocytes) cell model of acute myocardial infarction (AMI) was induced by 1% H/R. Quantitative reverse transcription-polymerase chain reaction was used to detect the expression levels of circ_0049271, miR-17-3p, and FZD4 in clinical blood samples and cells, and Cell Counting Kit-8 (CCK-8) was used to determine the proliferation rate of the cells in each group. Next, flow cytometry and Western blot were used to evaluate cell apoptosis. Biochemical tests and enzyme-linked immunosorbent assays (ELISAs) were then used to determine the activities/levels of the cell damage markers [i.e., creatine kinase (CK) and lactate dehydrogenase (LDH)], oxidative stress substances [i.e., malondialdehyde (MDA), reactive oxygen species (ROS), and superoxide dismutase (SOD)], and inflammatory factors [i.e., interleukin (IL)-1β, IL-6, and IL-8]. In addition, intermolecular interactions were verified using dual-luciferase reporter and RNA pull-down experiments.
UNASSIGNED: Circ_0049271 was significantly upregulated in both the blood of the AMI patients and the H/R-induced H9c2 cells. The knockdown of circ_0049271 increased the cell proliferation rate, decreased the apoptosis rate, inhibited oxidative stress (ROS and MDA were upregulated, and SOD was downregulated) and inflammatory responses (IL-1, IL-6, and IL-8 were downregulated), and relieved cell damage. However, the overexpression of circ_0049271 promoted H/R-induced H9c2 cell damage. Further experiments showed that miR-17-3p was a target of circ_0049271, and miR-17-3p was negatively correlated with circ_0049271 in the AMI blood samples. Additionally, miR-17-3p was found to target FZD4. A further exploration also revealed that miR-17-3p knockdown or FZD4 overexpression reversed the effects of si-circ_0049271 on the H/R-induced H9c2 cells; that is, miR-17-3p knockdown or FZD4 overexpression promoted H/R-induced injury in the H9c2 cells.
UNASSIGNED: Circ_0049271 promoted cellular function damage (e.g., proliferation inhibition, apoptosis, oxidative stress, and inflammation) in H/R-induced H9c2 cardiomyocytes via the miR-17-3p/FZD4 signaling axis.
摘要：
UNASSIGNED：本研究旨在探讨circ_0049271在缺氧-复氧（H/R）诱导的心肌细胞损伤中的作用和分子机制。
UNASSIGNED:使用维恩图鉴定了基因表达Omnibus(GEO)数据集中显著上调的环状核糖核酸(circRNAs)。1％H/R诱导急性心肌梗死（AMI）的H9c2（大鼠心肌细胞）细胞模型。定量逆转录-聚合酶链反应检测circ_0049271,miR-17-3p,和临床血液样本和细胞中的FZD4，用细胞计数试剂盒-8(CCK-8)测定各组细胞的增殖率。接下来,流式细胞术和Westernblot用于评估细胞凋亡。然后使用生化测试和酶联免疫吸附测定（ELISA）来确定细胞损伤标志物的活性/水平[即，肌酸激酶（CK）和乳酸脱氢酶（LDH）]，氧化应激物质[即，丙二醛（MDA），活性氧（ROS），和超氧化物歧化酶（SOD）]，和炎症因子[即，白细胞介素（IL）-1β，IL-6和IL-8]。此外,使用双荧光素酶报告基因和RNA下拉实验验证了分子间的相互作用。
UNASSIGNED：Circ_0049271在AMI患者的血液和H/R诱导的H9c2细胞中均显著上调。circ_0049271的敲除增加了细胞的增殖率，降低细胞凋亡率，抑制氧化应激(ROS和MDA上调，和SOD下调）和炎症反应（IL-1，IL-6和IL-8下调），减轻了细胞损伤。然而,circ_0049271的过表达促进了H/R诱导的H9c2细胞损伤。进一步的实验表明miR-17-3p是circ_0049271的靶标,在AMI血液样本中miR-17-3p与circ_0049271呈负相关。此外,发现miR-17-3p靶向FZD4。进一步的探索还揭示了miR-17-3p敲低或FZD4过表达逆转了si-circ_0049271对H/R诱导的H9c2细胞的作用；miR-17-3p敲低或FZD4过表达促进H/R诱导的H9c2细胞损伤。
未经授权：Circ_0049271促进了细胞功能损伤（例如，增殖抑制，凋亡，氧化应激，和炎症）通过miR-17-3p/FZD4信号轴在H/R诱导的H9c2心肌细胞中。
UNASSIGNED:使用维恩图鉴定了基因表达Omnibus(GEO)数据集中显著上调的环状核糖核酸(circRNAs)。
UNASSIGNED：Circ_0049271在AMI患者的血液和H/R诱导的H9c2细胞中均显著上调。
未经授权：Circ_0049271促进了细胞功能损伤（例如，
