| pubmed-article:16374426 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16374426 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:16374426 | lifeskim:mentions | umls-concept:C0160420 | lld:lifeskim |
| pubmed-article:16374426 | lifeskim:mentions | umls-concept:C0128897 | lld:lifeskim |
| pubmed-article:16374426 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:16374426 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:16374426 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:16374426 | pubmed:dateCreated | 2005-12-23 | lld:pubmed |
| pubmed-article:16374426 | pubmed:abstractText | Diabetic nephropathy involves a renal inflammatory response induced by the diabetic milieu. Macrophages accumulate in diabetic kidneys in association with the local upregulation of monocyte chemoattractant protein-1 (MCP-1); however, the contribution of macrophages to renal injury and the importance of MCP-1 to their accrual are unclear. Therefore, we examined the progression of streptozotocin (STZ)-induced diabetic nephropathy in mice deficient in MCP-1 in order to explore the role of MCP-1-mediated macrophage accumulation in the development of diabetic kidney damage. Renal pathology was examined at 2, 8, 12 and 18 weeks after STZ treatment in MCP-1 intact (+/+) and deficient (-/-) mice with equivalent blood glucose and hemoglobin A1c levels. In MCP-1(+/+) mice, the development of diabetic nephropathy was associated with increased kidney MCP-1 production, which occurred mostly in tubules, consistent with our in vitro finding that elements of the diabetic milieu (high glucose and advanced glycation end products) directly stimulate tubular MCP-1 secretion. Diabetes of 18 weeks resulted in albuminuria and elevated plasma creatinine in MCP-1(+/+) mice, but these aspects of renal injury were largely suppressed in MCP-1(-/-) mice. Protection from nephropathy in diabetic MCP-1(-/-) mice was associated with marked reductions in glomerular and interstitial macrophage accumulation, histological damage and renal fibrosis. Diabetic MCP-1(-/-) mice also had a smaller proportion of kidney macrophages expressing markers of activation (inducible nitric oxide synthase or sialoadhesin) compared to diabetic MCP-1(+/+) mice. In conclusion, our study demonstrates that MCP-1-mediated macrophage accumulation and activation plays a critical role in the development of STZ-induced mouse diabetic nephropathy. | lld:pubmed |
| pubmed-article:16374426 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16374426 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16374426 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16374426 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16374426 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16374426 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16374426 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:16374426 | pubmed:issn | 0085-2538 | lld:pubmed |
| pubmed-article:16374426 | pubmed:author | pubmed-author:AtkinsR CRC | lld:pubmed |
| pubmed-article:16374426 | pubmed:author | pubmed-author:TeschG HGH | lld:pubmed |
| pubmed-article:16374426 | pubmed:author | pubmed-author:Nikolic-Pater... | lld:pubmed |
| pubmed-article:16374426 | pubmed:author | pubmed-author:ChowF YFY | lld:pubmed |
| pubmed-article:16374426 | pubmed:author | pubmed-author:OzolsEE | lld:pubmed |
| pubmed-article:16374426 | pubmed:author | pubmed-author:RollinB JBJ | lld:pubmed |
| pubmed-article:16374426 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16374426 | pubmed:volume | 69 | lld:pubmed |
| pubmed-article:16374426 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16374426 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16374426 | pubmed:pagination | 73-80 | lld:pubmed |
| pubmed-article:16374426 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:16374426 | pubmed:meshHeading | pubmed-meshheading:16374426... | lld:pubmed |
| pubmed-article:16374426 | pubmed:meshHeading | pubmed-meshheading:16374426... | lld:pubmed |
| pubmed-article:16374426 | pubmed:meshHeading | pubmed-meshheading:16374426... | lld:pubmed |
| pubmed-article:16374426 | pubmed:meshHeading | pubmed-meshheading:16374426... | lld:pubmed |
| pubmed-article:16374426 | pubmed:meshHeading | pubmed-meshheading:16374426... | lld:pubmed |
| pubmed-article:16374426 | pubmed:meshHeading | pubmed-meshheading:16374426... | lld:pubmed |
| pubmed-article:16374426 | pubmed:meshHeading | pubmed-meshheading:16374426... | lld:pubmed |
| pubmed-article:16374426 | pubmed:meshHeading | pubmed-meshheading:16374426... | lld:pubmed |
| pubmed-article:16374426 | pubmed:meshHeading | pubmed-meshheading:16374426... | lld:pubmed |
| pubmed-article:16374426 | pubmed:meshHeading | pubmed-meshheading:16374426... | lld:pubmed |
| pubmed-article:16374426 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16374426 | pubmed:articleTitle | Monocyte chemoattractant protein-1 promotes the development of diabetic renal injury in streptozotocin-treated mice. | lld:pubmed |
| pubmed-article:16374426 | pubmed:affiliation | Department of Nephrology, Monash Medical Centre, Clayton, Victoria, Australia. | lld:pubmed |
| pubmed-article:16374426 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16374426 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:20296 | entrezgene:pubmed | pubmed-article:16374426 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16374426 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16374426 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16374426 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16374426 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16374426 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16374426 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16374426 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16374426 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16374426 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16374426 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16374426 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16374426 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16374426 | lld:pubmed |
