Effect of CASC15 on apoptosis and oxidative stress of cardiomyocytes after hypoxia/reperfusion injury
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 myocardi...
| Main Authors: | , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2024-02-01
|
| Series: | Revista Portuguesa de Cardiologia |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0870255123003918 |
| _version_ | 1797326324097875968 |
|---|---|
| author | Shuai Sun Xue Mei |
| author_facet | Shuai Sun Xue Mei |
| author_sort | Shuai Sun |
| collection | DOAJ |
| description | 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. Resumo: 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 expostas a hipóxia/reoxigenação (H/R) foram selecionadas como modelo para estudar os mecanismos envolvidos no enfarto 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. |
| first_indexed | 2024-03-08T06:21:42Z |
| format | Article |
| id | doaj.art-c48eb62e1dfc46c786ddf99c836a04db |
| institution | Directory Open Access Journal |
| issn | 0870-2551 |
| language | English |
| last_indexed | 2024-03-08T06:21:42Z |
| publishDate | 2024-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Revista Portuguesa de Cardiologia |
| spelling | doaj.art-c48eb62e1dfc46c786ddf99c836a04db2024-02-04T04:43:45ZengElsevierRevista Portuguesa de Cardiologia0870-25512024-02-014327784Effect of CASC15 on apoptosis and oxidative stress of cardiomyocytes after hypoxia/reperfusion injuryShuai Sun0Xue Mei1Emergency Medicine Clinical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing, ChinaCorresponding author.; Emergency Medicine Clinical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing, ChinaIntroduction 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. Resumo: 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 expostas a hipóxia/reoxigenação (H/R) foram selecionadas como modelo para estudar os mecanismos envolvidos no enfarto 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.http://www.sciencedirect.com/science/article/pii/S0870255123003918Hipóxia/reperfusãoTensão oxidativaCASC15MiR-542-3pEnfarte do miocárdio |
| spellingShingle | Shuai Sun Xue Mei Effect of CASC15 on apoptosis and oxidative stress of cardiomyocytes after hypoxia/reperfusion injury Revista Portuguesa de Cardiologia Hipóxia/reperfusão Tensão oxidativa CASC15 MiR-542-3p Enfarte do miocárdio |
| title | Effect of CASC15 on apoptosis and oxidative stress of cardiomyocytes after hypoxia/reperfusion injury |
| title_full | Effect of CASC15 on apoptosis and oxidative stress of cardiomyocytes after hypoxia/reperfusion injury |
| title_fullStr | Effect of CASC15 on apoptosis and oxidative stress of cardiomyocytes after hypoxia/reperfusion injury |
| title_full_unstemmed | Effect of CASC15 on apoptosis and oxidative stress of cardiomyocytes after hypoxia/reperfusion injury |
| title_short | Effect of CASC15 on apoptosis and oxidative stress of cardiomyocytes after hypoxia/reperfusion injury |
| title_sort | effect of casc15 on apoptosis and oxidative stress of cardiomyocytes after hypoxia reperfusion injury |
| topic | Hipóxia/reperfusão Tensão oxidativa CASC15 MiR-542-3p Enfarte do miocárdio |
| url | http://www.sciencedirect.com/science/article/pii/S0870255123003918 |
| work_keys_str_mv | AT shuaisun effectofcasc15onapoptosisandoxidativestressofcardiomyocytesafterhypoxiareperfusioninjury AT xuemei effectofcasc15onapoptosisandoxidativestressofcardiomyocytesafterhypoxiareperfusioninjury |