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http://purl.uniprot.org/citations/17259380http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17259380http://www.w3.org/2000/01/rdf-schema#comment"Microinflammation is a common major mechanism in the pathogenesis of diabetic vascular complications, including diabetic nephropathy. Macrophage scavenger receptor-A (SR-A) is a multifunctional receptor expressed on macrophages. This study aimed to determine the role of SR-A in diabetic nephropathy using SR-A-deficient (SR-A(-/-)) mice. Diabetes was induced in SR-A(-/-) and wild-type (SR-A(+/+)) mice by streptozotocin injection. Diabetic SR-A(+/+) mice presented characteristic features of diabetic nephropathy: albuminuria, glomerular hypertrophy, mesangial matrix expansion, and overexpression of transforming growth factor-beta at 6 months after induction of diabetes. These changes were markedly diminished in diabetic SR-A(-/-) mice, without differences in blood glucose and blood pressure levels. Interestingly, macrophage infiltration in the kidneys was dramatically decreased in diabetic SR-A(-/-) mice compared with diabetic SR-A(+/+) mice. DNA microarray revealed that proinflammatory genes were overexpressed in renal cortex of diabetic SR-A(+/+) mice and suppressed in diabetic SR-A(-/-) mice. Moreover, anti-SR-A antibody blocked the attachment of monocytes to type IV collagen substratum but not to endothelial cells. Our results suggest that SR-A promotes macrophage migration into diabetic kidneys by accelerating the attachment to renal extracellular matrices. SR-A may be a key molecule for the inflammatory process in pathogenesis of diabetic nephropathy and a novel therapeutic target for diabetic vascular complications."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.org/dc/terms/identifier"doi:10.2337/db06-0359"xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Kodama T."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Makino H."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Okada S."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Matsuda M."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Sasaki M."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Takeya M."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Kido Y."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Horiuchi S."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Ogawa D."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Ohga S."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Wada J."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Shikata K."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Tone A."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Shikata Y."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Nagase R."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Takeya M.'"xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Usui H.K."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/author"Yozai K."xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/name"Diabetes"xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/pages"363-372"xsd:string
http://purl.uniprot.org/citations/17259380http://purl.uniprot.org/core/title"Macrophage scavenger receptor-a-deficient mice are resistant against diabetic nephropathy through amelioration of microinflammation."xsd:string