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http://purl.uniprot.org/citations/22499991http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22499991http://www.w3.org/2000/01/rdf-schema#comment"

Objective

MicroRNAs (miRs) regulate angiogenesis by posttranscriptional silencing of target genes. The significance of angiostatic miR-200b in switching on skin wound angiogenesis was tested.

Methods and results

Wounding caused imminent and transient downregulation of miR-200b in dermal wound-edge endothelial cells. Derailing this injury response by lentiviral delivery of miR-200b in vivo impaired wound angiogenesis. Computational prediction, target reporter luciferase assay, and Western blot analysis provided first evidence that miR-200b targets globin transcription factor binding protein 2 (GATA2) and vascular endothelial growth factor receptor 2 (VEGFR2). Overexpression of GATA2 or VEGFR2 in endothelial cells rescued the angiostatic effect of miR-200b in vitro. Downregulation of miR-200b derepressed GATA2 and VEGFR2 expression to switch on wound angiogenesis, which was disrupted in diabetic wounds. Treatment of endothelial cells with tumor necrosis factor-α, a proinflammatory cytokine abundant in diabetic wounds, induced miR-200b expression, silenced GATA2 and VEGFR2, and suppressed angiogenesis. These outcomes were attenuated using anti-miR-200b strategy. Neutralization of tumor necrosis factor-α in the diabetic wounds improved wound angiogenesis and closure, which was accompanied by downregulation of miR-200b expression and desilencing of GATA2 and VEGFR2.

Conclusions

Injury-induced repression of miR-200b turned on wound angiogenesis. In mice with diabetes mellitus,excessive tumor necrosis factor-α induced miR-200b blunting proangiogenic functions of GATA2 and VEGFR2."xsd:string
http://purl.uniprot.org/citations/22499991http://purl.org/dc/terms/identifier"doi:10.1161/atvbaha.112.248583"xsd:string
http://purl.uniprot.org/citations/22499991http://purl.uniprot.org/core/author"Roy S."xsd:string
http://purl.uniprot.org/citations/22499991http://purl.uniprot.org/core/author"Khanna S."xsd:string
http://purl.uniprot.org/citations/22499991http://purl.uniprot.org/core/author"Chan Y.C."xsd:string
http://purl.uniprot.org/citations/22499991http://purl.uniprot.org/core/author"Sen C.K."xsd:string
http://purl.uniprot.org/citations/22499991http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22499991http://purl.uniprot.org/core/name"Arterioscler Thromb Vasc Biol"xsd:string
http://purl.uniprot.org/citations/22499991http://purl.uniprot.org/core/pages"1372-1382"xsd:string
http://purl.uniprot.org/citations/22499991http://purl.uniprot.org/core/title"Downregulation of endothelial microRNA-200b supports cutaneous wound angiogenesis by desilencing GATA binding protein 2 and vascular endothelial growth factor receptor 2."xsd:string
http://purl.uniprot.org/citations/22499991http://purl.uniprot.org/core/volume"32"xsd:string
http://purl.uniprot.org/citations/22499991http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22499991
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http://purl.uniprot.org/uniprot/P01375#attribution-9630739DAE7E844A87786A3F94A04182http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/22499991
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http://purl.uniprot.org/uniprot/#_Q3B845-mappedCitation-22499991http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22499991
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