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LncRNA CYTOR attenuates sepsis‐induced myocardial injury via regulating miR‐24/XIAP
Cell Biochemistry and Function ( IF 2.8 ) Pub Date : 2020-03-17 , DOI: 10.1002/cbf.3524
Ting Chen 1 , Chunyan Zhu 2 , Chongyang Ye 2
Affiliation  

This work aims to investigate the function and mechanism of long non‐coding RNA (lncRNA) cytoskeleton regulator RNA (CYTOR) in myocardial injury induced by sepsis. The sepsis‐induced myocardial injury model in mice was established by intraperitoneal injection of LPS (10 mg/kg) in vivo, and cardiomyocyte H9c2 was treated with LPS to mimic sepsis in vitro. CYTOR expression and miR‐24 expression were detected by qRT‐PCR. After up‐regulation or down‐regulation of CYTOR and miR‐24 expression in the H9c2 cells, and the viability of the cells was detected via MTT assay, and cell apoptosis was detected by TUNEL assay. Western blot was applied to determine the expression level of caspase 3, Bax and X‐chromosome‐linked inhibitor of apoptosis (XIAP). Interaction between CYTOR and miR‐24 was determined by bioinformatics analysis, RT‐PCR and dual luciferase reporter assay. Interaction between miR‐24 and XIAP was determined through bioinformatics analysis, RT‐PCR, western blot and dual luciferase reporter assay. CYTOR was markedly down‐regulated. CYTOR interacted with miR‐24, and negatively regulated its expression level. Over‐expression of CYTOR or transfection of miR‐24 inhibitors significantly promoted viability and inhibited apoptosis of H9c2 cells, while the knockdown of CYTOR and transfection of miR‐24 mimics had opposite effects. CYTOR suppressed the expression level of apoptosis‐related proteins, but miR‐24 increased them. miR‐24 directly targeted the 3'UTR of XIAP, and suppressed it, and XIAP was modulated indirectly by CYTOR. Down‐regulation of CYTOR aggravates sepsis‐induced cardiac injury via regulating miR‐24 and XIAP.

中文翻译:

LncRNA CYTOR通过调节miR-24 / XIAP减轻败血症诱导的心肌损伤

这项工作旨在研究败血症诱导的心肌损伤中长非编码RNA(lncRNA)细胞骨架调节剂RNA(CYTOR)的功能和机制。通过在体内腹膜内注射LPS(10 mg / kg)建立败血症诱发的小鼠心肌损伤模型,并用LPS处理心肌细胞H9c2以在体外模拟败血症。通过qRT-PCR检测CYTOR和miR-24的表达。在H9c2细胞中CYTOR和miR-24表达的上调或下调后,通过MTT分析检测细胞活力,并通过TUNEL分析检测细胞凋亡。应用蛋白质印迹法测定caspase 3,Bax和X染色体连锁的凋亡抑制剂(XIAP)的表达水平。CYTOR和miR-24之间的相互作用是通过生物信息学分析确定的,RT‐PCR和双重萤光素酶报告基因检测 miR-24和XIAP之间的相互作用是通过生物信息学分析,RT-PCR,western印迹和双重荧光素酶报告基因分析确定的。CYTOR明显下调。CYTOR与miR-24相互作用,并负调控其表达水平。CYTOR的过表达或miR-24抑制剂的转染可显着提高H9c2细胞的活力并抑制其凋亡,而CYTOR的敲除和miR-24模仿物的转染则具有相反的作用。CYTOR抑制凋亡相关蛋白的表达水平,但miR-24却增加了它们的表达。miR-24直接靶向并抑制了XIAP的3'UTR,而XIAP被CYTOR间接调节。CYTOR的下调通过调节miR-24和XIAP加剧了败血症诱发的心脏损伤。miR-24和XIAP之间的相互作用是通过生物信息学分析,RT-PCR,western印迹和双重荧光素酶报告基因分析确定的。CYTOR明显下调。CYTOR与miR-24相互作用,并负面调节其表达水平。CYTOR的过表达或miR-24抑制剂的转染可显着提高H9c2细胞的活力并抑制其凋亡,而CYTOR的敲除和miR-24模仿物的转染则具有相反的作用。CYTOR抑制凋亡相关蛋白的表达水平,但miR-24却增加了它们的表达。miR-24直接靶向并抑制了XIAP的3'UTR,而XIAP被CYTOR间接调节。CYTOR的下调通过调节miR-24和XIAP加剧了败血症诱发的心脏损伤。miR-24和XIAP之间的相互作用是通过生物信息学分析,RT-PCR,western印迹和双重荧光素酶报告基因分析确定的。CYTOR明显下调。CYTOR与miR-24相互作用,并负调控其表达水平。CYTOR的过表达或miR-24抑制剂的转染可显着提高H9c2细胞的活力并抑制其凋亡,而CYTOR的敲除和miR-24模仿物的转染则具有相反的作用。CYTOR抑制凋亡相关蛋白的表达水平,但miR-24却增加了它们的表达。miR-24直接靶向并抑制了XIAP的3'UTR,而XIAP被CYTOR间接调节。CYTOR的下调通过调节miR-24和XIAP加剧了败血症诱发的心脏损伤。免疫印迹和双重荧光素酶报告基因检测。CYTOR明显下调。CYTOR与miR-24相互作用,并负调控其表达水平。CYTOR的过表达或miR-24抑制剂的转染显着提高了H9c2细胞的活力并抑制了H9c2细胞的凋亡,而CYTOR的敲除和miR-24模仿物的转染则具有相反的作用。CYTOR抑制凋亡相关蛋白的表达水平,但miR-24却增加了它们的表达。miR-24直接靶向并抑制了XIAP的3'UTR,而XIAP被CYTOR间接调节。CYTOR的下调通过调节miR-24和XIAP加剧了败血症诱发的心脏损伤。免疫印迹和双重荧光素酶报告基因检测。CYTOR明显下调。CYTOR与miR-24相互作用,并负调控其表达水平。CYTOR的过表达或miR-24抑制剂的转染可显着提高H9c2细胞的活力并抑制其凋亡,而CYTOR的敲除和miR-24模仿物的转染则具有相反的作用。CYTOR抑制凋亡相关蛋白的表达水平,但miR-24却增加了它们的表达。miR-24直接靶向并抑制了XIAP的3'UTR,而XIAP被CYTOR间接调节。CYTOR的下调通过调节miR-24和XIAP加剧了败血症诱发的心脏损伤。CYTOR的过表达或miR-24抑制剂的转染可显着提高H9c2细胞的活力并抑制其凋亡,而CYTOR的敲除和miR-24模仿物的转染则具有相反的作用。CYTOR抑制凋亡相关蛋白的表达水平,但miR-24却增加了它们的表达。miR-24直接靶向并抑制了XIAP的3'UTR,而XIAP被CYTOR间接调节。CYTOR的下调通过调节miR-24和XIAP加剧了败血症诱发的心脏损伤。CYTOR的过表达或miR-24抑制剂的转染显着提高了H9c2细胞的活力并抑制了H9c2细胞的凋亡,而CYTOR的敲除和miR-24模仿物的转染则具有相反的作用。CYTOR抑制凋亡相关蛋白的表达水平,但miR-24却增加了它们的表达。miR-24直接靶向并抑制了XIAP的3'UTR,而XIAP被CYTOR间接调节。CYTOR的下调通过调节miR-24和XIAP加剧了败血症诱发的心脏损伤。并抑制它,而XIAP被CYTOR间接调节。CYTOR的下调通过调节miR-24和XIAP加剧了败血症诱发的心脏损伤。并抑制它,而XIAP被CYTOR间接调节。CYTOR的下调通过调节miR-24和XIAP加剧了败血症诱发的心脏损伤。
更新日期:2020-03-17
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