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MicroRNA-210-mediated proliferation, survival, and angiogenesis promote cardiac repair post myocardial infarction in rodents
dc.contributor.author | Arif, Mohammed | |
dc.contributor.author | Pandey, Raghav | |
dc.contributor.author | Alam, Perwez | |
dc.contributor.author | Jiang, Shujia | |
dc.contributor.author | Sadayappan, Sakthivel | |
dc.contributor.author | Paul, Arghya | |
dc.contributor.author | Ahmed, Rafeeq P. H. | |
dc.date.accessioned | 2018-06-07T19:37:36Z | |
dc.date.available | 2018-06-07T19:37:36Z | |
dc.date.issued | 2017-12 | |
dc.identifier.citation | Arif, M., Pandey, R., Alam, P., Jiang, S., Sadayappan, S., Paul, A., & Ahmed, R. P. H. (2017). MicroRNA-210-mediated proliferation, survival, and angiogenesis promote cardiac repair post myocardial infarction in rodents. Journal of Molecular Medicine (Berlin, Germany), 95(12), 1369–1385. http://doi.org/10.1007/s00109-017-1591-8 | en_US |
dc.identifier.uri | http://hdl.handle.net/1808/26461 | |
dc.description | The final publication is available at Springer via http://dx.doi.org/10.1007/s00109-017-1591-8. | en_US |
dc.description.abstract | An innovative approach for cardiac regeneration following injury is to induce endogenous cardiomyocyte (CM) cell cycle re-entry. In the present study, CMs from adult rat hearts were isolated and transfected with cel-miR-67 (control) and rno-miR-210. A significant increase in CM proliferation and mono-nucleation were observed in miR-210 group, in addition to a reduction in CM size, multi-nucleation, and cell death. When compared to control, β-catenin and Bcl-2 were upregulated while APC (adenomatous polyposis coli), p16, and caspase-3 were downregulated in miR-210 group. In silico analysis predicted cell cycle inhibitor, APC, as a direct target of miR-210 in rodents. Moreover, compared to control, a significant increase in CM survival and proliferation were observed with siRNA-mediated inhibition of APC. Furthermore, miR-210 overexpressing C57BL/6 mice (210-TG) were used for short-term ischemia/reperfusion study, revealing smaller cell size, increased mono-nucleation, decreased multi-nucleation, and increased CM proliferation in 210-TG hearts in contrast to wild-type (NTG). Likewise, myocardial infarction (MI) was created in adult mice, echocardiography was performed, and the hearts were harvested for immunohistochemistry and molecular studies. Compared to NTG, 210-TG hearts showed a significant increase in CM proliferation, reduced apoptosis, upregulated angiogenesis, reduced infarct size, and overall improvement in cardiac function following MI. β-catenin, Bcl-2, and VEGF (vascular endothelial growth factor) were upregulated while APC, p16, and caspase-3 were downregulated in 210-TG hearts. Overall, constitutive overexpression of miR-210 rescues heart function following cardiac injury in adult mice via promoting CM proliferation, cell survival, and angiogenesis. | en_US |
dc.publisher | Springer Verlag | en_US |
dc.subject | MiR-210 | en_US |
dc.subject | Cardiomyocyte | en_US |
dc.subject | Adenomatous polyposis coli | en_US |
dc.subject | Myocardial infarction | en_US |
dc.title | MicroRNA-210-mediated proliferation, survival, and angiogenesis promote cardiac repair post myocardial infarction in rodents | en_US |
dc.type | Article | en_US |
kusw.kuauthor | Arghya, Paul | |
kusw.kudepartment | Chemical and Petroleum Engineering | en_US |
dc.identifier.doi | 10.1007/s00109-017-1591-8 | en_US |
kusw.oaversion | Scholarly/refereed, publisher version | en_US |
kusw.oapolicy | This item meets KU Open Access policy criteria. | en_US |
dc.rights.accessrights | openAccess |