{"title":"LncRNA-Fendrr：参与核仁素对H2O2诱导的心肌细胞损伤的保护作用。","authors":"Cheng Chen, Xiaofang Lin, Yuting Tang, Hui Sun, Leijing Yin, Zhengyang Luo, Shuxin Wang, Pengfei Liang, Bimei Jiang","doi":"10.1080/13510002.2023.2168626","DOIUrl":null,"url":null,"abstract":"<p><p><b>Background:</b> Nucleolin is a multifunctional nucleolar protein with RNA-binding properties. Increased nucleolin expression protects cells from H<sub>2</sub>O<sub>2</sub>-induced damage, but the mechanism remains unknown. Long noncoding RNAs (lncRNAs) play crucial roles in cardiovascular diseases. However, the biological functions and underlying mechanisms of lncRNAs in myocardial injury remain unclear.<b>Methods:</b> In a nucleolin-overexpressing cardiac cell line, high-throughput technology was used to identify lncRNAs controlled by nucleolin. Cell counting kit-8 assay was used to determine cell viability, lactate dehydrogenase (LDH) assay to detect cell death, caspase activity assay and propidium iodide staining to confirm cell apoptosis, and RNA immunoprecipitation to examine the interaction between Fendrr and nucleolin.<b>Results:</b> We found that Fendrr expression was significantly downregulated in mouse hearts subjected to myocardial ischemia-reperfusion (MI/R) injury. High Fendrr expression abrogated H<sub>2</sub>O<sub>2</sub>-mediated injury in cardiomyocytes as evidenced by increased cell viability and decreased cell apoptosis. Conversely, Fendrr knockdown exacerbated the cardiomyocytes injury. Also, nucleolin overexpression inhibits Fendrr downregulation in H<sub>2</sub>O<sub>2</sub>-induced cardiomyocyte injury. Fendrr overexpression significantly reversed the role of the suppression of nucleolin expression in H<sub>2</sub>O<sub>2</sub>-induced cardiomyocytes.<b>Conclusion:</b> LncRNA Fendrr is involved in the cardioprotective effect of nucleolin against H<sub>2</sub>O<sub>2</sub>-induced injury and may be a potential therapeutic target for oxidative stress-induced myocardial injury.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"28 1","pages":"2168626"},"PeriodicalIF":5.2000,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9891159/pdf/","citationCount":"1","resultStr":"{\"title\":\"LncRNA Fendrr: involvement in the protective role of nucleolin against H<sub>2</sub>O<sub>2</sub>-induced injury in cardiomyocytes.\",\"authors\":\"Cheng Chen, Xiaofang Lin, Yuting Tang, Hui Sun, Leijing Yin, Zhengyang Luo, Shuxin Wang, Pengfei Liang, Bimei Jiang\",\"doi\":\"10.1080/13510002.2023.2168626\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p><b>Background:</b> Nucleolin is a multifunctional nucleolar protein with RNA-binding properties. Increased nucleolin expression protects cells from H<sub>2</sub>O<sub>2</sub>-induced damage, but the mechanism remains unknown. Long noncoding RNAs (lncRNAs) play crucial roles in cardiovascular diseases. However, the biological functions and underlying mechanisms of lncRNAs in myocardial injury remain unclear.<b>Methods:</b> In a nucleolin-overexpressing cardiac cell line, high-throughput technology was used to identify lncRNAs controlled by nucleolin. Cell counting kit-8 assay was used to determine cell viability, lactate dehydrogenase (LDH) assay to detect cell death, caspase activity assay and propidium iodide staining to confirm cell apoptosis, and RNA immunoprecipitation to examine the interaction between Fendrr and nucleolin.<b>Results:</b> We found that Fendrr expression was significantly downregulated in mouse hearts subjected to myocardial ischemia-reperfusion (MI/R) injury. High Fendrr expression abrogated H<sub>2</sub>O<sub>2</sub>-mediated injury in cardiomyocytes as evidenced by increased cell viability and decreased cell apoptosis. Conversely, Fendrr knockdown exacerbated the cardiomyocytes injury. Also, nucleolin overexpression inhibits Fendrr downregulation in H<sub>2</sub>O<sub>2</sub>-induced cardiomyocyte injury. Fendrr overexpression significantly reversed the role of the suppression of nucleolin expression in H<sub>2</sub>O<sub>2</sub>-induced cardiomyocytes.<b>Conclusion:</b> LncRNA Fendrr is involved in the cardioprotective effect of nucleolin against H<sub>2</sub>O<sub>2</sub>-induced injury and may be a potential therapeutic target for oxidative stress-induced myocardial injury.</p>\",\"PeriodicalId\":21096,\"journal\":{\"name\":\"Redox Report\",\"volume\":\"28 1\",\"pages\":\"2168626\"},\"PeriodicalIF\":5.2000,\"publicationDate\":\"2023-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9891159/pdf/\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Redox Report\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1080/13510002.2023.2168626\",\"RegionNum\":2,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Redox Report","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/13510002.2023.2168626","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
LncRNA Fendrr: involvement in the protective role of nucleolin against H2O2-induced injury in cardiomyocytes.
Background: Nucleolin is a multifunctional nucleolar protein with RNA-binding properties. Increased nucleolin expression protects cells from H2O2-induced damage, but the mechanism remains unknown. Long noncoding RNAs (lncRNAs) play crucial roles in cardiovascular diseases. However, the biological functions and underlying mechanisms of lncRNAs in myocardial injury remain unclear.Methods: In a nucleolin-overexpressing cardiac cell line, high-throughput technology was used to identify lncRNAs controlled by nucleolin. Cell counting kit-8 assay was used to determine cell viability, lactate dehydrogenase (LDH) assay to detect cell death, caspase activity assay and propidium iodide staining to confirm cell apoptosis, and RNA immunoprecipitation to examine the interaction between Fendrr and nucleolin.Results: We found that Fendrr expression was significantly downregulated in mouse hearts subjected to myocardial ischemia-reperfusion (MI/R) injury. High Fendrr expression abrogated H2O2-mediated injury in cardiomyocytes as evidenced by increased cell viability and decreased cell apoptosis. Conversely, Fendrr knockdown exacerbated the cardiomyocytes injury. Also, nucleolin overexpression inhibits Fendrr downregulation in H2O2-induced cardiomyocyte injury. Fendrr overexpression significantly reversed the role of the suppression of nucleolin expression in H2O2-induced cardiomyocytes.Conclusion: LncRNA Fendrr is involved in the cardioprotective effect of nucleolin against H2O2-induced injury and may be a potential therapeutic target for oxidative stress-induced myocardial injury.
期刊介绍：
Redox Report is a multidisciplinary peer-reviewed open access journal focusing on the role of free radicals, oxidative stress, activated oxygen, perioxidative and redox processes, primarily in the human environment and human pathology. Relevant papers on the animal and plant environment, biology and pathology will also be included.
While emphasis is placed upon methodological and intellectual advances underpinned by new data, the journal offers scope for review, hypotheses, critiques and other forms of discussion.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
