Exosome-mediated targeted delivery of miR-210 for angiogenic therapy after cerebral ischemia in mice
Abstract Background Accumulating evidence shows that microRNA-210 (miR-210) holds great promise to improve angiogenesis for brain tissue repair after cerebral ischemia. However, safe and efficient delivery of miR-210 via intravenous administration is still a challenge. In the past decade, exosomes h...
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Format: | Article |
Language: | English |
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BMC
2019-02-01
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Series: | Journal of Nanobiotechnology |
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Online Access: | http://link.springer.com/article/10.1186/s12951-019-0461-7 |
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author | Huixin Zhang Jin Wu Jiahuan Wu Qi Fan Jingchao Zhou Junwen Wu Sichen Liu Jie Zang Jinhai Ye Ming Xiao Tian Tian Jun Gao |
author_facet | Huixin Zhang Jin Wu Jiahuan Wu Qi Fan Jingchao Zhou Junwen Wu Sichen Liu Jie Zang Jinhai Ye Ming Xiao Tian Tian Jun Gao |
author_sort | Huixin Zhang |
collection | DOAJ |
description | Abstract Background Accumulating evidence shows that microRNA-210 (miR-210) holds great promise to improve angiogenesis for brain tissue repair after cerebral ischemia. However, safe and efficient delivery of miR-210 via intravenous administration is still a challenge. In the past decade, exosomes have emerged as a novel endogenous delivery system. Here, c(RGDyK) peptide is conjugated to exosomes, and they are loaded with cholesterol-modified miR-210 (RGD-exo:miR-210). Results In a transient middle cerebral artery occlusion (MCAO) mouse model, the RGD-exo:miR-210 targets the lesion region of the ischemic brain after intravenous administration, resulting in an increase in miR-210 at the site. Furthermore, RGD-exo:miR-210 are administered once every other day for 14 days, and the expressions of integrin β3, vascular endothelial growth factor (VEGF) and CD34 are significantly upregulated. The animal survival rate is also enhanced. Conclusions These results suggest a strategy for the targeted delivery of miR-210 to ischemic brain and provide an angiogenic agent for the treatment of ischemic stroke. |
first_indexed | 2024-04-11T22:31:19Z |
format | Article |
id | doaj.art-a52e965a50fd4eb3854314159eba7088 |
institution | Directory Open Access Journal |
issn | 1477-3155 |
language | English |
last_indexed | 2024-04-11T22:31:19Z |
publishDate | 2019-02-01 |
publisher | BMC |
record_format | Article |
series | Journal of Nanobiotechnology |
spelling | doaj.art-a52e965a50fd4eb3854314159eba70882022-12-22T03:59:25ZengBMCJournal of Nanobiotechnology1477-31552019-02-0117111310.1186/s12951-019-0461-7Exosome-mediated targeted delivery of miR-210 for angiogenic therapy after cerebral ischemia in miceHuixin Zhang0Jin Wu1Jiahuan Wu2Qi Fan3Jingchao Zhou4Junwen Wu5Sichen Liu6Jie Zang7Jinhai Ye8Ming Xiao9Tian Tian10Jun Gao11The Department of Neurobiology, Key Laboratory of Human Functional Genomics of Jiangsu, Nanjing Medical UniversityThe Department of Neurology, The Second Affiliated Hospital of Nanjing Medical UniversityThe Department of Neurobiology, Key Laboratory of Human Functional Genomics of Jiangsu, Nanjing Medical UniversityThe School of Basic Medical Science, Nanjing Medical UniversityThe School of Basic Medical Science, Nanjing Medical UniversityThe School of Basic Medical Science, Nanjing Medical UniversityThe School of Basic Medical Science, Nanjing Medical UniversityThe School of Basic Medical Science, Nanjing Medical UniversityThe Department of Oral and Maxillofacial Surgery, The Affiliated Stomatology Hospital of Nanjing Medical University, Nanjing Medical UniversityJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical UniversityThe Department of Neurobiology, Key Laboratory of Human Functional Genomics of Jiangsu, Nanjing Medical UniversityThe Department of Neurobiology, Key Laboratory of Human Functional Genomics of Jiangsu, Nanjing Medical UniversityAbstract Background Accumulating evidence shows that microRNA-210 (miR-210) holds great promise to improve angiogenesis for brain tissue repair after cerebral ischemia. However, safe and efficient delivery of miR-210 via intravenous administration is still a challenge. In the past decade, exosomes have emerged as a novel endogenous delivery system. Here, c(RGDyK) peptide is conjugated to exosomes, and they are loaded with cholesterol-modified miR-210 (RGD-exo:miR-210). Results In a transient middle cerebral artery occlusion (MCAO) mouse model, the RGD-exo:miR-210 targets the lesion region of the ischemic brain after intravenous administration, resulting in an increase in miR-210 at the site. Furthermore, RGD-exo:miR-210 are administered once every other day for 14 days, and the expressions of integrin β3, vascular endothelial growth factor (VEGF) and CD34 are significantly upregulated. The animal survival rate is also enhanced. Conclusions These results suggest a strategy for the targeted delivery of miR-210 to ischemic brain and provide an angiogenic agent for the treatment of ischemic stroke.http://link.springer.com/article/10.1186/s12951-019-0461-7IschemiamiR-210ExosomesAngiogenesis |
spellingShingle | Huixin Zhang Jin Wu Jiahuan Wu Qi Fan Jingchao Zhou Junwen Wu Sichen Liu Jie Zang Jinhai Ye Ming Xiao Tian Tian Jun Gao Exosome-mediated targeted delivery of miR-210 for angiogenic therapy after cerebral ischemia in mice Journal of Nanobiotechnology Ischemia miR-210 Exosomes Angiogenesis |
title | Exosome-mediated targeted delivery of miR-210 for angiogenic therapy after cerebral ischemia in mice |
title_full | Exosome-mediated targeted delivery of miR-210 for angiogenic therapy after cerebral ischemia in mice |
title_fullStr | Exosome-mediated targeted delivery of miR-210 for angiogenic therapy after cerebral ischemia in mice |
title_full_unstemmed | Exosome-mediated targeted delivery of miR-210 for angiogenic therapy after cerebral ischemia in mice |
title_short | Exosome-mediated targeted delivery of miR-210 for angiogenic therapy after cerebral ischemia in mice |
title_sort | exosome mediated targeted delivery of mir 210 for angiogenic therapy after cerebral ischemia in mice |
topic | Ischemia miR-210 Exosomes Angiogenesis |
url | http://link.springer.com/article/10.1186/s12951-019-0461-7 |
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