http://purl.uniprot.org/citations/25656649 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/25656649 | http://www.w3.org/2000/01/rdf-schema#comment | "More and more miRNAs have been shown to regulate gene expression in the heart and dysregulation of their expression has been linked to cardiovascular diseases including the miR-199a/214 cluster. However, the signature of circulating miR-214 expression and its possible roles during the development of heart failure has been less well studied. In this study, we elucidated the biological and clinical significance of miR-214 dysregulation in heart failure. Firstly, circulating miR-214 was measured by quantitative PCR, and we found that miR-214 was upregulated in the serum of chronic heart failure patients, as well as in hypertrophic and failing hearts of humans and mice. Adeno-associated virus serotype 9 (AAV9)-mediated miR-214 silencing attenuates isoproterenol (ISO) infusion-induced cardiac dysfunction and impairment of cardiac angiogenesis in mice. Mechanistically, miR-214 overexpression reduces angiogenesis of HUVECs by targeting XBP1, an important transcription factor of unfolded protein response, and XBP1 silencing decreases HUVECs proliferation and angiogenesis similar to miR-214 overexpression. Furthermore, ectopic expression of XBP1 enhances endothelial cells proliferation and tube formation, and reverses anti-angiogenic effect of miR-214 over expression. All these findings suggest that miR-214 is an important regulator of angiogenesis in heart in vitro and in vivo, likely via regulating the expression of XBP1, and demonstrate that miR-214 plays an essential role in the control/inhibition of cardiac angiogenesis."xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.org/dc/terms/identifier | "doi:10.1002/jcp.24942"xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/author | "Chen C."xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/author | "Gong W."xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/author | "Wang F."xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/author | "Yang L."xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/author | "Wang P."xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/author | "Duan Q."xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/author | "Wang D.W."xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/author | "Zou M.H."xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/author | "Chaugai S."xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/name | "J Cell Physiol"xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/pages | "1964-1973"xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/title | "MicroRNA-214 Is Upregulated in Heart Failure Patients and Suppresses XBP1-Mediated Endothelial Cells Angiogenesis."xsd:string |
http://purl.uniprot.org/citations/25656649 | http://purl.uniprot.org/core/volume | "230"xsd:string |
http://purl.uniprot.org/citations/25656649 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/25656649 |
http://purl.uniprot.org/citations/25656649 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/25656649 |
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http://purl.uniprot.org/uniprot/P17861#attribution-4736B98E30800D9A7FD8CCE5C0CBA0EE | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/25656649 |
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http://purl.uniprot.org/uniprot/#_P17861-mappedCitation-25656649 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/25656649 |
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