miR-200a-5p regulates myocardial necroptosis induced by Se deficiency via targeting RNF11
Necroptosis has been discovered as a new paradigm of cell death and may play a key role in heart disease and selenium (Se) deficiency. Hence, we detected the specific microRNA (miRNA) in response to Se-deficient heart using microRNAome analysis. For high-throughput sequencing using Se-deficient chic...
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| Format: | Article |
| Language: | English |
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Elsevier
2018-05-01
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| Series: | Redox Biology |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2213231717307711 |
| _version_ | 1811288751068938240 |
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| author | Tianshu Yang Changyu Cao Jie Yang Tianqi Liu Xin Gen Lei Ziwei Zhang Shiwen Xu |
| author_facet | Tianshu Yang Changyu Cao Jie Yang Tianqi Liu Xin Gen Lei Ziwei Zhang Shiwen Xu |
| author_sort | Tianshu Yang |
| collection | DOAJ |
| description | Necroptosis has been discovered as a new paradigm of cell death and may play a key role in heart disease and selenium (Se) deficiency. Hence, we detected the specific microRNA (miRNA) in response to Se-deficient heart using microRNAome analysis. For high-throughput sequencing using Se-deficient chicken cardiac tissue, we selected miR-200a-5p and its target gene ring finger protein 11 (RNF11) based on differential expression in cardiac tissue and confirmed the relationship between miR-200a-5p and RNF11 by dual luciferase reporter assay and real-time quantitative PCR (qRT-PCR) in cardiomyocytes. We further explored the function of miR-200a-5p and observed that overexpression of miR-200a-5p spark the receptor interacting serine/threonine kinase 3 (RIP3)-dependent necroptosis in vivo and in vitro. To understand whether miR-200a-5p and RNF11 are involved in the RIP3-dependent necroptosis pathway, we presumed that oxidative stress, inflammation response and the mitogen-activated protein kinase (MAPK) pathway might trigger necroptosis. Interestingly, necroptosis trigger, z-VAD-fmk, failed to induce necroptosis but enhanced cell survival against necrosis in cardiomyocytes with knockdown of miR-200a-5p. Our present study provides a new insight that the modulation of miR-200a-5p and its target gene might block necroptosis in the heart, revealing a novel myocardial necrosis regulation model in heart disease. |
| first_indexed | 2024-04-13T03:42:43Z |
| format | Article |
| id | doaj.art-82d0c7fbff5443a5bb0828e7ef50bb66 |
| institution | Directory Open Access Journal |
| issn | 2213-2317 |
| language | English |
| last_indexed | 2024-04-13T03:42:43Z |
| publishDate | 2018-05-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Redox Biology |
| spelling | doaj.art-82d0c7fbff5443a5bb0828e7ef50bb662022-12-22T03:04:06ZengElsevierRedox Biology2213-23172018-05-0115C15916910.1016/j.redox.2017.11.025miR-200a-5p regulates myocardial necroptosis induced by Se deficiency via targeting RNF11Tianshu Yang0Changyu Cao1Jie Yang2Tianqi Liu3Xin Gen Lei4Ziwei Zhang5Shiwen Xu6Northeast Agricultural University, Harbin 150030, PR ChinaNortheast Agricultural University, Harbin 150030, PR ChinaNortheast Agricultural University, Harbin 150030, PR ChinaNortheast Agricultural University, Harbin 150030, PR ChinaDepartment of Animal Science, Cornell University, Ithaca, NY, United StatesNortheast Agricultural University, Harbin 150030, PR ChinaNortheast Agricultural University, Harbin 150030, PR ChinaNecroptosis has been discovered as a new paradigm of cell death and may play a key role in heart disease and selenium (Se) deficiency. Hence, we detected the specific microRNA (miRNA) in response to Se-deficient heart using microRNAome analysis. For high-throughput sequencing using Se-deficient chicken cardiac tissue, we selected miR-200a-5p and its target gene ring finger protein 11 (RNF11) based on differential expression in cardiac tissue and confirmed the relationship between miR-200a-5p and RNF11 by dual luciferase reporter assay and real-time quantitative PCR (qRT-PCR) in cardiomyocytes. We further explored the function of miR-200a-5p and observed that overexpression of miR-200a-5p spark the receptor interacting serine/threonine kinase 3 (RIP3)-dependent necroptosis in vivo and in vitro. To understand whether miR-200a-5p and RNF11 are involved in the RIP3-dependent necroptosis pathway, we presumed that oxidative stress, inflammation response and the mitogen-activated protein kinase (MAPK) pathway might trigger necroptosis. Interestingly, necroptosis trigger, z-VAD-fmk, failed to induce necroptosis but enhanced cell survival against necrosis in cardiomyocytes with knockdown of miR-200a-5p. Our present study provides a new insight that the modulation of miR-200a-5p and its target gene might block necroptosis in the heart, revealing a novel myocardial necrosis regulation model in heart disease.http://www.sciencedirect.com/science/article/pii/S2213231717307711SeleniumNecroptosisCardiomyocytesmiR-200a-5pRNF11 |
| spellingShingle | Tianshu Yang Changyu Cao Jie Yang Tianqi Liu Xin Gen Lei Ziwei Zhang Shiwen Xu miR-200a-5p regulates myocardial necroptosis induced by Se deficiency via targeting RNF11 Redox Biology Selenium Necroptosis Cardiomyocytes miR-200a-5p RNF11 |
| title | miR-200a-5p regulates myocardial necroptosis induced by Se deficiency via targeting RNF11 |
| title_full | miR-200a-5p regulates myocardial necroptosis induced by Se deficiency via targeting RNF11 |
| title_fullStr | miR-200a-5p regulates myocardial necroptosis induced by Se deficiency via targeting RNF11 |
| title_full_unstemmed | miR-200a-5p regulates myocardial necroptosis induced by Se deficiency via targeting RNF11 |
| title_short | miR-200a-5p regulates myocardial necroptosis induced by Se deficiency via targeting RNF11 |
| title_sort | mir 200a 5p regulates myocardial necroptosis induced by se deficiency via targeting rnf11 |
| topic | Selenium Necroptosis Cardiomyocytes miR-200a-5p RNF11 |
| url | http://www.sciencedirect.com/science/article/pii/S2213231717307711 |
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