Naringenin promotes angiogenesis of ischemic myocardium after myocardial infarction through miR-223-3p/IGF1R axis
Introduction: Naringenin exerts a protective effect on myocardial ischemia and reperfusion. It has been reported that miR-223-3p is a potential target for the treatment of myocardial infarction (MI). In view of the unreported correlation between Naringenin and miR-223-3p, this study was designed to...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2022-12-01
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| Series: | Regenerative Therapy |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2352320422000761 |
| _version_ | 1811188458118447104 |
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| author | Jinguo Fu Heping Niu Guangren Gao Lei Wang Kai Yu Run Guo Jun Zhang |
| author_facet | Jinguo Fu Heping Niu Guangren Gao Lei Wang Kai Yu Run Guo Jun Zhang |
| author_sort | Jinguo Fu |
| collection | DOAJ |
| description | Introduction: Naringenin exerts a protective effect on myocardial ischemia and reperfusion. It has been reported that miR-223-3p is a potential target for the treatment of myocardial infarction (MI). In view of the unreported correlation between Naringenin and miR-223-3p, this study was designed to confirm that the ameliorative effects of Naringenin on MI is directly related to the regulation of miR-223-3p. Methods: Through electrocardiogram detection, Masson pathological staining and immunohistochemistry of angiogenesis-related factors, alleviative effects of Naringenin on heart function, myocardial injury and angiogenesis in MI mice were observed individually. Hypoxic HUVECs were selected in the in vitro experimental model. The cell viability, angiogenesis and migration ability were analyzed to fathom out the pro-angiogenesis potential of Naringenin. The effect of Naringenin on miR-223-3p, as well as the downstream molecular mechanism was verified through bioinformatics analysis and rescue experiments. Results: Naringenin improved heart functions of MI mice, reduced degree of myocardial fibrosis, stimulated expressions of angiogenic factors and down-regulated level of miR-223-3p in myocardial tissue. In in vitro experiments, Naringenin increased the viability of hypoxic HUVECs, as well as the abilities of tube formation and migration, and further inhibited the expression of miR-223-3p. In the rescue trial, miR-223-3p mimic reversed the therapeutic effect of Naringenin. Type 1 insulin-like growth factor receptor (IGF1R), as a downstream target gene of miR-223-3p, partially offset the cellular regulatory effects of miR-223-3p after overexpression of IGF1R. Conclusions: Naringenin improves the angiogenesis of hypoxic HUVECs by regulating the miR-223-3p/IGF1R axis, and has the potential to promote myocardial angiogenesis in MI mice. |
| first_indexed | 2024-04-11T14:19:09Z |
| format | Article |
| id | doaj.art-76b83e99ff654cf6b128210104b9328c |
| institution | Directory Open Access Journal |
| issn | 2352-3204 |
| language | English |
| last_indexed | 2024-04-11T14:19:09Z |
| publishDate | 2022-12-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Regenerative Therapy |
| spelling | doaj.art-76b83e99ff654cf6b128210104b9328c2022-12-22T04:19:07ZengElsevierRegenerative Therapy2352-32042022-12-0121362371Naringenin promotes angiogenesis of ischemic myocardium after myocardial infarction through miR-223-3p/IGF1R axisJinguo Fu0Heping Niu1Guangren Gao2Lei Wang3Kai Yu4Run Guo5Jun Zhang6Department of Cardiology, Cangzhou Central Hospital, ChinaDepartment of Cardiology, Cangzhou Central Hospital, ChinaDepartment of Cardiology, Cangzhou Central Hospital, ChinaDepartment of Cardiology, Cangzhou Central Hospital, ChinaDepartment of Cardiology, Cangzhou Central Hospital, ChinaDepartment of Cardiology, Cangzhou Central Hospital, ChinaCorresponding author. Department of Cardiology, Cangzhou Central Hospital, 16 Xinhua West Road, Cangzhou City, Hebei Province, 061001, China.; Department of Cardiology, Cangzhou Central Hospital, ChinaIntroduction: Naringenin exerts a protective effect on myocardial ischemia and reperfusion. It has been reported that miR-223-3p is a potential target for the treatment of myocardial infarction (MI). In view of the unreported correlation between Naringenin and miR-223-3p, this study was designed to confirm that the ameliorative effects of Naringenin on MI is directly related to the regulation of miR-223-3p. Methods: Through electrocardiogram detection, Masson pathological staining and immunohistochemistry of angiogenesis-related factors, alleviative effects of Naringenin on heart function, myocardial injury and angiogenesis in MI mice were observed individually. Hypoxic HUVECs were selected in the in vitro experimental model. The cell viability, angiogenesis and migration ability were analyzed to fathom out the pro-angiogenesis potential of Naringenin. The effect of Naringenin on miR-223-3p, as well as the downstream molecular mechanism was verified through bioinformatics analysis and rescue experiments. Results: Naringenin improved heart functions of MI mice, reduced degree of myocardial fibrosis, stimulated expressions of angiogenic factors and down-regulated level of miR-223-3p in myocardial tissue. In in vitro experiments, Naringenin increased the viability of hypoxic HUVECs, as well as the abilities of tube formation and migration, and further inhibited the expression of miR-223-3p. In the rescue trial, miR-223-3p mimic reversed the therapeutic effect of Naringenin. Type 1 insulin-like growth factor receptor (IGF1R), as a downstream target gene of miR-223-3p, partially offset the cellular regulatory effects of miR-223-3p after overexpression of IGF1R. Conclusions: Naringenin improves the angiogenesis of hypoxic HUVECs by regulating the miR-223-3p/IGF1R axis, and has the potential to promote myocardial angiogenesis in MI mice.http://www.sciencedirect.com/science/article/pii/S2352320422000761Myocardial infarctionNaringeninType 1 insulin-like growth factor receptorRevascularizationMiR-223-3p |
| spellingShingle | Jinguo Fu Heping Niu Guangren Gao Lei Wang Kai Yu Run Guo Jun Zhang Naringenin promotes angiogenesis of ischemic myocardium after myocardial infarction through miR-223-3p/IGF1R axis Regenerative Therapy Myocardial infarction Naringenin Type 1 insulin-like growth factor receptor Revascularization MiR-223-3p |
| title | Naringenin promotes angiogenesis of ischemic myocardium after myocardial infarction through miR-223-3p/IGF1R axis |
| title_full | Naringenin promotes angiogenesis of ischemic myocardium after myocardial infarction through miR-223-3p/IGF1R axis |
| title_fullStr | Naringenin promotes angiogenesis of ischemic myocardium after myocardial infarction through miR-223-3p/IGF1R axis |
| title_full_unstemmed | Naringenin promotes angiogenesis of ischemic myocardium after myocardial infarction through miR-223-3p/IGF1R axis |
| title_short | Naringenin promotes angiogenesis of ischemic myocardium after myocardial infarction through miR-223-3p/IGF1R axis |
| title_sort | naringenin promotes angiogenesis of ischemic myocardium after myocardial infarction through mir 223 3p igf1r axis |
| topic | Myocardial infarction Naringenin Type 1 insulin-like growth factor receptor Revascularization MiR-223-3p |
| url | http://www.sciencedirect.com/science/article/pii/S2352320422000761 |
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