miR-34b/c regulates doxorubicin-induced myocardial cell injury through ITCH
Objective: To determine the underlying mechanism of miR-34b/c in regulating doxorubicin (Dox)-induced myocardial cell injury.Methods: The viability of mouse myocardial cells HL-1 was detected by MTT assay. The apoptosis of HL-1 cells was detected by TUNEL assay. mRNA expressions of ITCH, TNF-α and IL-6 were measured by qRT-PCR. Protein levels of ITCH, NF-κB, TNF-α and IL-6 were measured by western blot. Dual luciferase assay was performed to detect the regulation of miR-34b/c on ITCH. Mouse model of cardiomyopathy was induced by intraperitoneal injection of Dox.Results: Dox reduced HL-1 cell viability and activated NF-κB pathway in HL-1 cells. miR-34b/c expressions were gradually up-regulated and ITCH expression was gradually down-regulated in Dox-treated HL-1 cells. miR-34b/c expression had negative correlation with the mRNA expression of ITCH. Besides, ITCH was a target of miR-34b/c. miR-34b/c mimic reduced cell viability, suppressed ITCH expression, increased TNF-α and IL-6 level, and promoted NF-κB expression in nucleus and cytoplasm of HL-1 cells. Whereas silencing miR-34 protected HL-1 cells through regulating ITCH. Finally, we demonstrated miR-34 antagomir-protected myocardial cells in mouse model of cardiomyopathy.Conclusion: miR-34b/c decreased HL-1 cell viability and promoted the secretion of proinflammatory cytokines in Dox-induced myocardial cells through ITCH/NF-κB pathway.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2019 |
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| Erschienen: |
2019 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:18 |
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| Enthalten in: |
Cell cycle (Georgetown, Tex.) - 18(2019), 23 vom: 18. Dez., Seite 3263-3274 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Zhang, Wen-Cai [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 18.09.2020 Date Revised 18.10.2020 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1080/15384101.2019.1673618 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM302340505 |
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| 100 | 1 | |a Zhang, Wen-Cai |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a miR-34b/c regulates doxorubicin-induced myocardial cell injury through ITCH |
| 264 | 1 | |c 2019 | |
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| 500 | |a Date Revised 18.10.2020 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Objective: To determine the underlying mechanism of miR-34b/c in regulating doxorubicin (Dox)-induced myocardial cell injury.Methods: The viability of mouse myocardial cells HL-1 was detected by MTT assay. The apoptosis of HL-1 cells was detected by TUNEL assay. mRNA expressions of ITCH, TNF-α and IL-6 were measured by qRT-PCR. Protein levels of ITCH, NF-κB, TNF-α and IL-6 were measured by western blot. Dual luciferase assay was performed to detect the regulation of miR-34b/c on ITCH. Mouse model of cardiomyopathy was induced by intraperitoneal injection of Dox.Results: Dox reduced HL-1 cell viability and activated NF-κB pathway in HL-1 cells. miR-34b/c expressions were gradually up-regulated and ITCH expression was gradually down-regulated in Dox-treated HL-1 cells. miR-34b/c expression had negative correlation with the mRNA expression of ITCH. Besides, ITCH was a target of miR-34b/c. miR-34b/c mimic reduced cell viability, suppressed ITCH expression, increased TNF-α and IL-6 level, and promoted NF-κB expression in nucleus and cytoplasm of HL-1 cells. Whereas silencing miR-34 protected HL-1 cells through regulating ITCH. Finally, we demonstrated miR-34 antagomir-protected myocardial cells in mouse model of cardiomyopathy.Conclusion: miR-34b/c decreased HL-1 cell viability and promoted the secretion of proinflammatory cytokines in Dox-induced myocardial cells through ITCH/NF-κB pathway | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Doxorubicin | |
| 650 | 4 | |a ITCH | |
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| 650 | 4 | |a miR-34b/c | |
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| 650 | 7 | |a NF-kappa B |2 NLM | |
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| 650 | 7 | |a Tumor Necrosis Factor-alpha |2 NLM | |
| 650 | 7 | |a Doxorubicin |2 NLM | |
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| 650 | 7 | |a Itch protein, mouse |2 NLM | |
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| 700 | 1 | |a Yang, Jin-Hua |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Guang-Hui |e verfasserin |4 aut | |
| 700 | 1 | |a Yang, Fan |e verfasserin |4 aut | |
| 700 | 1 | |a Gong, Jun-Long |e verfasserin |4 aut | |
| 700 | 1 | |a Jia, Meng-Ge |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Meng-Juan |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Luo-Sha |e verfasserin |4 aut | |
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