| http://purl.uniprot.org/citations/28948298 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/28948298 | http://www.w3.org/2000/01/rdf-schema#comment | "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.Key messagesMiRNA-210 transfected adult rat CMs show proliferation and reduced cell death in vitro. Cell cycle inhibitor APC is a target of miR-210. MiR-210 overexpressing (210-TG) mouse hearts show CMs cell cycle re-entry and survival post myocardial injury. 210-TG mice show significant neovascularization and angiogenic potential post myocardial infarction. 210-TG hearts show reduced infarct size following ischemic injury."xsd:string |
| http://purl.uniprot.org/citations/28948298 | http://purl.org/dc/terms/identifier | "doi:10.1007/s00109-017-1591-8"xsd:string |
| http://purl.uniprot.org/citations/28948298 | http://purl.uniprot.org/core/author | "Jiang S."xsd:string |
| http://purl.uniprot.org/citations/28948298 | http://purl.uniprot.org/core/author | "Pandey R."xsd:string |
| http://purl.uniprot.org/citations/28948298 | http://purl.uniprot.org/core/author | "Arif M."xsd:string |
| http://purl.uniprot.org/citations/28948298 | http://purl.uniprot.org/core/author | "Paul A."xsd:string |
| http://purl.uniprot.org/citations/28948298 | http://purl.uniprot.org/core/author | "Alam P."xsd:string |
| http://purl.uniprot.org/citations/28948298 | http://purl.uniprot.org/core/author | "Sadayappan S."xsd:string |
| http://purl.uniprot.org/citations/28948298 | http://purl.uniprot.org/core/author | "Ahmed R.P.H."xsd:string |
| http://purl.uniprot.org/citations/28948298 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/28948298 | http://purl.uniprot.org/core/name | "J Mol Med (Berl)"xsd:string |
| http://purl.uniprot.org/citations/28948298 | http://purl.uniprot.org/core/pages | "1369-1385"xsd:string |
| http://purl.uniprot.org/citations/28948298 | http://purl.uniprot.org/core/title | "MicroRNA-210-mediated proliferation, survival, and angiogenesis promote cardiac repair post myocardial infarction in rodents."xsd:string |
| http://purl.uniprot.org/citations/28948298 | http://purl.uniprot.org/core/volume | "95"xsd:string |
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