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http://purl.uniprot.org/citations/25255225http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25255225http://www.w3.org/2000/01/rdf-schema#comment"Vasohibin-1 (VASH1) is a unique endogenous inhibitor of angiogenesis that is induced in endothelial cells by pro-angiogenic factors. We previously reported renoprotective effect of adenoviral delivery of VASH1 in diabetic nephropathy model, and herein investigated the potential protective role of endogenous VASH1 by using VASH1-deficient mice. Streptozotocin-induced type 1 diabetic VASH1 heterozygous knockout mice (VASH1(+/-)) or wild-type diabetic mice were sacrificed 16 weeks after inducing diabetes. In the diabetic VASH1(+/-) mice, albuminuria were significantly exacerbated compared with the diabetic wild-type littermates, in association with the dysregulated distribution of glomerular slit diaphragm related proteins, nephrin and ZO-1, glomerular basement membrane thickening and reduction of slit diaphragm density. Glomerular monocyte/macrophage infiltration and glomerular nuclear translocation of phosphorylated NF-κB p65 were significantly exacerbated in the diabetic VASH1(+/-) mice compared with the diabetic wild-type littermates, accompanied by the augmentation of VEGF-A, M1 macrophage-derived MCP-1 and phosphorylation of IκBα, and the decrease of angiopoietin-1/2 ratio and M2 macrophage-derived Arginase-1. The glomerular CD31(+) endothelial area was also increased in the diabetic VASH1(+/-) mice compared with the diabetic-wild type littermates. Furthermore, the renal and glomerular hypertrophy, glomerular accumulation of mesangial matrix and type IV collagen and activation of renal TGF-β1/Smad3 signaling, a key mediator of renal fibrosis, were exacerbated in the diabetic VASH1(+/-) mice compared with the diabetic wild-type littermates. In conditionally immortalized mouse podocytes cultured under high glucose condition, transfection of VASH1 small interfering RNA (siRNA) resulted in the reduction of nephrin, angiopoietin-1 and ZO-1, and the augmentation of VEGF-A compared with control siRNA. These results suggest that endogenous VASH1 may regulate the development of diabetic renal alterations, partly via direct effects on podocytes, and thus, a strategy to recover VASH1 might potentially lead to the development of a novel therapeutic approach for diabetic nephropathy."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0107934"xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/author"Makino H."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/author"Sato Y."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/author"Masuda K."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/author"Tanabe K."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/author"Saito D."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/author"Sugiyama H."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/author"Nasu T."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/author"Arata Y."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/author"Yamasaki H."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/author"Maeshima Y."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/author"Ujike H."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/author"Hinamoto N."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/author"Watatani H."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/name"PLoS One"xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/pages"e107934"xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/title"Exacerbation of diabetic renal alterations in mice lacking vasohibin-1."xsd:string
http://purl.uniprot.org/citations/25255225http://purl.uniprot.org/core/volume"9"xsd:string
http://purl.uniprot.org/citations/25255225http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25255225
http://purl.uniprot.org/citations/25255225http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25255225
http://purl.uniprot.org/uniprot/#_A0PCF8-mappedCitation-25255225http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25255225
http://purl.uniprot.org/uniprot/#_Q0VGS1-mappedCitation-25255225http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25255225
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