| http://purl.uniprot.org/citations/23060436 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23060436 | http://www.w3.org/2000/01/rdf-schema#comment | "miR-199a-5p plays a critical role in controlling cardiomyocyte survival. However, its significance in endothelial cell biology remains ambiguous. Here, we report the first evidence that miR-199a-5p negatively regulates angiogenic responses by directly targeting v-ets erythroblastosis virus E26 oncogene homolog 1 (Ets-1). Induction of miR-199a-5p in human dermal microvascular endothelial cells (HMECs) blocked angiogenic response in Matrigel® culture, whereas miR-199a-5p-deprived cells exhibited enhanced angiogenesis in vitro. Bioinformatics prediction and miR target reporter assay recognized Ets-1 as a novel direct target of miR-199a-5p. Delivery of miR-199a-5p blocked Ets-1 expression in HMECs, whereas knockdown endogenous miR-199a-5p induced Ets-1 expression. Matrix metalloproteinase 1 (MMP-1), one of the Ets-1 downstream mediators, was negatively regulated by miR-199a-5p. Overexpression of Ets-1 not only rescued miR-199a-5p-dependent anti-angiogenic effects but also reversed miR-199a-5p-induced loss of MMP-1 expression. Similarly, Ets-1 knockdown blunted angiogenic response and induction of MMP-1 in miR-199a-5p-deprived HMECs. Examination of cutaneous wound dermal tissue revealed a significant down-regulation of miR-199a-5p expression, which was associated with induction of Ets-1 and MMP-1. Mice carrying homozygous deletions in the Ets-1 gene exhibited blunted wound blood flow and reduced abundance of endothelial cells. Impaired wound angiogenesis was associated with compromised wound closure, insufficient granulation tissue formation, and blunted induction of MMP-1. Thus, down-regulation of miR-199a-5p is involved in the induction of wound angiogenesis through derepressing of the Ets-1-MMP1 pathway."xsd:string |
| http://purl.uniprot.org/citations/23060436 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m112.413294"xsd:string |
| http://purl.uniprot.org/citations/23060436 | http://purl.uniprot.org/core/author | "Huang Y."xsd:string |
| http://purl.uniprot.org/citations/23060436 | http://purl.uniprot.org/core/author | "Roy S."xsd:string |
| http://purl.uniprot.org/citations/23060436 | http://purl.uniprot.org/core/author | "Khanna S."xsd:string |
| http://purl.uniprot.org/citations/23060436 | http://purl.uniprot.org/core/author | "Chan Y.C."xsd:string |
| http://purl.uniprot.org/citations/23060436 | http://purl.uniprot.org/core/author | "Sen C.K."xsd:string |
| http://purl.uniprot.org/citations/23060436 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/23060436 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/23060436 | http://purl.uniprot.org/core/pages | "41032-41043"xsd:string |
| http://purl.uniprot.org/citations/23060436 | http://purl.uniprot.org/core/title | "The microRNA miR-199a-5p down-regulation switches on wound angiogenesis by derepressing the v-ets erythroblastosis virus E26 oncogene homolog 1-matrix metalloproteinase-1 pathway."xsd:string |
| http://purl.uniprot.org/citations/23060436 | http://purl.uniprot.org/core/volume | "287"xsd:string |
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