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• W4386248082 abstract "Introduction and Objectives: The increasing incidence of ischemic heart disease is a serious threat to human health. Increased CASC15, a long non-coding RNA, has been shown to adversely affect cardiac muscle. The objective of this paper was to explore the effect of CASC15 on a cell model of myocardial infarction and its possible mechanism. Methods: H9c2 cells were selected to establish the myocardial infarction model through hypoxia/reoxygenation (H/R) treatment. The expression of CASC15 was attenuated by cell transfection in vitro. The level of CASC15 was detected by RT-qPCR. Cell viability was detected by CCK-8 assay, and cell apoptosis was assessed by flow cytometry. The content of MDA and the activity of SOD and GSH-Px were measured by ELISA. Luciferase reporter gene assay was used to determine the relationship between CASC15 and miRNA. Results: CASC15 expression was increased in H/R-treated H9c2 cells. Overexpression of CASC15 adversely affected cell viability and promoted H/R-induced oxidative stress. Inhibition of CASC15 promoted cell viability and suppressed cell apoptosis and oxidative stress damage. Additionally, luciferase reporter gene assay confirmed the targeting relationship between CASC15 and miR-542-3p, and attenuating CASC15 expression enhanced the level of miR-542-3p. Reduction of miR-542-3p weakened the viability of the H/R cell model, increased apoptosis, and enhanced oxidative stress damage. Conclusion: This study suggests that overexpression of CASC15 may inhibit the viability of H9c2 cells, promote apoptosis and induce oxidative stress through targeted regulation of miR-542-3p expression. Introdução e Objetivos: O aumento da doença isquémica cardíaca representa uma séria ameaça à saúde humana. Um aumento no CASC15, um RNA não codificante longo, está associado à lesão do músculo cardíaco. O objetivo deste trabalho foi explorar o mecanismo celular através do qual a CASC15 contribui para o enfarte do miocárdio. Métodos: Células H9c2 exposta a hipóxia/reoxigenação (H/R) foram selecionadas como modelo para estudar os mecanismos envolvidos no infarto do miocárdio. A expressão de CASC15 foi inibida pela transfecção com siRNA. Os níveis de CASC15 foram avaliados por RT-qPCR e a viabilidade celular e apoptose determinadas pelo ensaio CCK-8 e citometria de fluxo, respetivamente. Os teores de MDA, SOD e GSH-Px foram medidos por ELISA. O ensaio do gene repórter da luciferase foi utilizado para verificar a relação entre CASC15 e os níveis do miRNA miR-542-3p. Resultados: Células H9c2 sujeitas a H/R apresentam níveis aumentados de CASC15. A sobre-expressão de CASC15 afetou negativamente a função celular e promoveu a lesão induzida pelo stress associado H/R. Por outro lado, a inibição do CASC15 promoveu viabilidade celular e suprimiu apoptose celular e os danos oxidativos. Além disso, o ensaio do gene repórter da luciferase confirmou a relação alvo entre CASC15 e miR-542-3p, com uma diminuição da expressão de CASC15 a resultar num aumento do nível de miR-542-3p. Uma diminuição do miR-542-3p comprometeu a viabilidade do modelo de células H/R e aumentou a apoptose e o dano oxidativo. Conclusão: Este estudo sugere que um aumento da expressão de CASC15 durante a H/R pode contribuir para diminuir a viabilidade dos cardiomiócitos, promover apoptose e induzir stress oxidativo, através da regulação da expressão de miR-542-3p." @default.
• W4386248082 created "2023-08-30" @default.
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• W4386248082 date "2023-08-01" @default.
• W4386248082 modified "2023-10-17" @default.
• W4386248082 title "Effect of CASC15 on apoptosis and oxidative stress of cardiomyocytes after hypoxia/reperfusion injury" @default.
• W4386248082 doi "https://doi.org/10.1016/j.repc.2023.04.017" @default.
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