RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/22843786http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22843786http://www.w3.org/2000/01/rdf-schema#comment"

Rationale

Related transcriptional enhancer factor-1 (RTEF-1) plays an important role in endothelial cell function by regulating angiogenesis; however, the mechanism underlying the role of RTEF-1 in the endothelium in vivo is not well defined.

Objective

We investigated the biological functions of RTEF-1 by disrupting the gene that encodes it in mice endothelium -specific RTEF-1-deficient transgenic mice (RTEF-1(-/-)).

Methods and results

RTEF-1(-/-) mice showed significantly increased blood glucose levels and insulin resistance, accompanied by decreased levels of insulin-like growth factor binding protein-1 (IGFBP-1) mRNA in the endothelium and decreased serum IGFBP-1 levels. Additionally, the RTEF-1(-/-) phenotype was exacerbated when the mice were fed a high-fat diet, which correlated with decreased IGFBP-1 levels. In contrast, vascular endothelial cadherin/RTEF-1-overexpressing(1) transgenic mice (VE-Cad/RTEF1) demonstrated improved glucose clearance and insulin sensitivity in response to a high-fat diet. Furthermore, we demonstrated that RTEF-1 upregulates IGFBP-1 through selective binding and promotion of transcription from the insulin response element site. Insulin prevented RTEF-1 expression and significantly inhibited IGFBP-1 transcription in endothelial cells in a dose-dependent fashion.

Conclusions

To the best of our knowledge, this is the first report demonstrating that RTEF-1 stimulates promoter activity through an insulin response element and also mediates the effects of insulin on gene expression. These results show that RTEF-1-stimulated IGFBP-1 expression may be central to the mechanism by which RTEF-1 attenuates blood glucose levels. These findings provide the basis for novel insights into the transcriptional regulation of IGFBP-1 and contribute to our understanding of the role of vascular endothelial cells in metabolism."xsd:string
http://purl.uniprot.org/citations/22843786http://purl.org/dc/terms/identifier"doi:10.1161/circresaha.112.268110"xsd:string
http://purl.uniprot.org/citations/22843786http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/22843786http://purl.uniprot.org/core/author"Guo S."xsd:string
http://purl.uniprot.org/citations/22843786http://purl.uniprot.org/core/author"Wu J."xsd:string
http://purl.uniprot.org/citations/22843786http://purl.uniprot.org/core/author"He P."xsd:string
http://purl.uniprot.org/citations/22843786http://purl.uniprot.org/core/author"Messmer-Blust A.F."xsd:string
http://purl.uniprot.org/citations/22843786http://purl.uniprot.org/core/author"Philbrick M.J."xsd:string
http://purl.uniprot.org/citations/22843786http://purl.uniprot.org/core/author"Guo S.'"xsd:string
http://purl.uniprot.org/citations/22843786http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22843786http://purl.uniprot.org/core/name"Circ Res"xsd:string
http://purl.uniprot.org/citations/22843786http://purl.uniprot.org/core/pages"991-1001"xsd:string
http://purl.uniprot.org/citations/22843786http://purl.uniprot.org/core/title"RTEF-1 attenuates blood glucose levels by regulating insulin-like growth factor binding protein-1 in the endothelium."xsd:string
http://purl.uniprot.org/citations/22843786http://purl.uniprot.org/core/volume"111"xsd:string
http://purl.uniprot.org/citations/22843786http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22843786
http://purl.uniprot.org/citations/22843786http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22843786
http://purl.uniprot.org/uniprot/#_Q15561-mappedCitation-22843786http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22843786
http://purl.uniprot.org/uniprot/#_A0A0R4IZY5-mappedCitation-22843786http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22843786
http://purl.uniprot.org/uniprot/#_A0A0R4J1U4-mappedCitation-22843786http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22843786
http://purl.uniprot.org/uniprot/#_A0A0S2Z4E5-mappedCitation-22843786http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22843786
http://purl.uniprot.org/uniprot/#_A0A0S2Z4F2-mappedCitation-22843786http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22843786
http://purl.uniprot.org/uniprot/#_F6UKF4-mappedCitation-22843786http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22843786
http://purl.uniprot.org/uniprot/#_F6ULG6-mappedCitation-22843786http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22843786
http://purl.uniprot.org/uniprot/#_D3DUQ6-mappedCitation-22843786http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22843786