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http://purl.uniprot.org/citations/21885851http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21885851http://www.w3.org/2000/01/rdf-schema#comment"

Objective

MicroRNAs play key roles in modulating a variety of cellular processes by posttranscriptional regulation of their target genes. Vascular endothelial growth factor (VEGF), VEGF receptor-2 (VEGFR2), and fibroblast growth factor receptor-1 (FGFR1) were identified by bioinformatic approaches and subsequently validated as targets of microRNA (miR)-16 and miR-424 in endothelial cells (ECs).

Methods and results

Mimetics of these microRNAs reduced VEGF, VEGFR2, and FGFR1 expression, whereas specific antagonists enhanced their expression. Expression of mature miR-16 and miR-424 was upregulated on VEGF or basic fibroblast growth factor (bFGF) treatment. This upregulation was accompanied by a parallel increase in primary transcript (pri-miR)-16-1 and pri-miR-16-2 but not in pri-miR-424 levels, indicating a VEGF/bFGF-dependent transcriptional and posttranscriptional regulation of miR-16 and miR-424, respectively. Reduced expression of VEGFR2 and FGFR1 by miR-16 or miR-424 overexpression regulated VEGF and bFGF signaling through these receptors, thereby affecting the activity of downstream components of the pathways. Functionally, miR-16 or miR-424 overexpression reduced proliferation, migration, and cord formation of ECs in vitro, and lentiviral overexpression of miR-16 reduced the ability of ECs to form blood vessels in vivo.

Conclusion

We conclude that these miRNAs fine-tune the expression of selected endothelial angiogenic mediators in response to these growth factors. Altogether, these findings suggest that miR-16 and miR-424 play important roles in regulating cell-intrinsic angiogenic activity of ECs."xsd:string
http://purl.uniprot.org/citations/21885851http://purl.org/dc/terms/identifier"doi:10.1161/atvbaha.111.236521"xsd:string
http://purl.uniprot.org/citations/21885851http://purl.uniprot.org/core/author"Sandhu D."xsd:string
http://purl.uniprot.org/citations/21885851http://purl.uniprot.org/core/author"Fernandez-Hernando C."xsd:string
http://purl.uniprot.org/citations/21885851http://purl.uniprot.org/core/author"Araldi E."xsd:string
http://purl.uniprot.org/citations/21885851http://purl.uniprot.org/core/author"Suarez Y."xsd:string
http://purl.uniprot.org/citations/21885851http://purl.uniprot.org/core/author"Penalva L.O."xsd:string
http://purl.uniprot.org/citations/21885851http://purl.uniprot.org/core/author"Chamorro-Jorganes A."xsd:string
http://purl.uniprot.org/citations/21885851http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21885851http://purl.uniprot.org/core/name"Arterioscler Thromb Vasc Biol"xsd:string
http://purl.uniprot.org/citations/21885851http://purl.uniprot.org/core/pages"2595-2606"xsd:string
http://purl.uniprot.org/citations/21885851http://purl.uniprot.org/core/title"MicroRNA-16 and microRNA-424 regulate cell-autonomous angiogenic functions in endothelial cells via targeting vascular endothelial growth factor receptor-2 and fibroblast growth factor receptor-1."xsd:string
http://purl.uniprot.org/citations/21885851http://purl.uniprot.org/core/volume"31"xsd:string
http://purl.uniprot.org/citations/21885851http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21885851
http://purl.uniprot.org/citations/21885851http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21885851
http://purl.uniprot.org/uniprot/P11362#attribution-0BB5790609369CFBF376C5F1005173E5http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/21885851
http://purl.uniprot.org/uniprot/P35968#attribution-0BB5790609369CFBF376C5F1005173E5http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/21885851
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http://purl.uniprot.org/uniprot/#_A0A0H4A7S0-mappedCitation-21885851http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21885851
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