http://purl.uniprot.org/citations/21228103 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/21228103 | http://www.w3.org/2000/01/rdf-schema#comment | "The involvement of VEGF-A as well as the therapeutic efficacy of angiogenesis inhibitors in diabetic nephropathy have been reported. We recently reported the therapeutic effects of vasohibin-1 (VASH-1), an endogenous angiogenesis inhibitor, in a type 1 diabetic nephropathy model (Nasu T, Maeshima Y, Kinomura M, Hirokoshi-Kawahara K, Tanabe K, Sugiyama H, Sonoda H, Sato Y, Makino H. Diabetes 58: 2365-2375, 2009). In this study, we investigated the therapeutic efficacy of VASH-1 on renal alterations in obese mice with type 2 diabetes. Diabetic db/db mice received intravenous injections of adenoviral vectors encoding human VASH-1 (AdhVASH-1) and were euthanized 8 wk later. AdhVASH-1 treatment resulted in significant suppression of glomerular hypertrophy, glomerular hyperfiltration, albuminuria, increase in the CD31(+) glomerular endothelial area, F4/80(+) monocyte/macrophage infiltration, the accumulation of type IV collagen, and mesangial matrix. An increase in the renal levels of VEGF-A, VEGFR-2, transforming growth factor (TGF)-β1, and monocyte chemoattractant protein-1 in diabetic animals was significantly suppressed by AdhVASH-1 (immunoblotting). AdhVASH-1 treatment significantly recovered the loss and altered the distribution patterns of nephrin and zonula occludens (ZO)-1 and suppressed the increase in the number of fibroblast-specific protein-1 (FSP-1(+)) and desmin(+) podocytes in diabetic mice. In vitro, recombinant human VASH-1 (rhVASH-1) dose dependently suppressed the upregulation of VEGF induced by high ambient glucose (25 mM) in cultured mouse podocytes. In addition, rhVASH-1 significantly recovered the mRNA levels of nephrin and the protein levels of ZO-1 and P-cadherin and suppressed the increase in protein levels of desmin, FSP-1, Snail, and Slug in podocytes under high-glucose condition. Taken together, these results suggest the potential use of VASH-1 as a novel therapeutic agent in type 2 diabetic nephropathy mediated via antiangiogenic effects and maintenance of podocyte phenotype in association with antiproteinuric effects."xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajprenal.00503.2010"xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/author | "Makino H."xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/author | "Sato Y."xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/author | "Tanabe K."xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/author | "Saito D."xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/author | "Sugiyama H."xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/author | "Sonoda H."xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/author | "Nasu T."xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/author | "Yamasaki H."xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/author | "Maeshima Y."xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/name | "Am J Physiol Renal Physiol"xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/pages | "F873-86"xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/title | "Amelioration of renal alterations in obese type 2 diabetic mice by vasohibin-1, a negative feedback regulator of angiogenesis."xsd:string |
http://purl.uniprot.org/citations/21228103 | http://purl.uniprot.org/core/volume | "300"xsd:string |
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