Linked Life Data

16190318

Source:http://linkedlifedata.com/resource/pubmed/id/16190318

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2005-9-29
pubmed:abstractText
The aim of this study was to clarify the role of the renal renin-angiotensin system (RAS) in diabetic nephropathy (DN), which was induced by injection of streptozotocin (STZ). Male CBA/N and CBA/J mice were compared in this study. The former possesses a single renin gene, Ren1, whereas the latter carries two renin genes, Ren1 and Ren2. To examine the molecular dynamics of renal RAS, including renin, angiotensinogen (Agt), angiotensin-converting enzyme (Ace), angiotensin type 1 (Agtr1) and type 2 (Agtr2) receptors in experimental DN, we performed laser-microdissection (LMD) followed by reverse transcriptase nested polymerase chain reaction using each specific primer pairs and immunohistochemistry for renin and angiotensin II. CBA/N mice had a higher response after injection of STZ than CBA/J mice, showing a significant increase of the kidney/body weight ratio, although there was no significant difference between the two strains for the blood glucose level or pancreatic beta-cell response. The onset of renal pathological changes associated with DN was earlier and more severe in CBA/N mice than in CBA/J mice. Distinct immunoreactivities for renin and angiotensin II were newly distributed on the flattened epithelial cells in the dilated distal tubules in the cortex as well as the collecting ducts in the cortex and medulla, and were demonstrated more intensely in CBA/N mice than in CBA/J mice. Microdissectional analysis in both DN models revealed a higher incidence of RAS-related gene expression in CBA/J, Ren 1 Ren 2 mice than in CBA/N, Ren 1 mice. These findings suggest that intrarenal RAS plays an important role in the onset of renal pathological changes associated with DN. Additionally, Ren 1 mice have more severe histopathological nephropathy than Ren1 Ren2 mice, followed by marked production of angiotensin II.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0047-1917
pubmed:author
pubmed:issnType
Print
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
13-26
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:16190318-Angiotensin II, pubmed-meshheading:16190318-Angiotensinogen, pubmed-meshheading:16190318-Animals, pubmed-meshheading:16190318-Blood Glucose, pubmed-meshheading:16190318-Body Weight, pubmed-meshheading:16190318-Diabetes Mellitus, Experimental, pubmed-meshheading:16190318-Diabetic Nephropathies, pubmed-meshheading:16190318-Immunohistochemistry, pubmed-meshheading:16190318-Insulin, pubmed-meshheading:16190318-Kidney, pubmed-meshheading:16190318-Male, pubmed-meshheading:16190318-Mice, pubmed-meshheading:16190318-Mice, Inbred CBA, pubmed-meshheading:16190318-Mice, Inbred DBA, pubmed-meshheading:16190318-Mice, Inbred MRL lpr, pubmed-meshheading:16190318-Organ Size, pubmed-meshheading:16190318-RNA, Messenger, pubmed-meshheading:16190318-Receptors, Angiotensin, pubmed-meshheading:16190318-Renin, pubmed-meshheading:16190318-Renin-Angiotensin System, pubmed-meshheading:16190318-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16190318-Specific Pathogen-Free Organisms, pubmed-meshheading:16190318-Up-Regulation
pubmed:year
2005
pubmed:articleTitle
Upregulation of renal renin-angiotensin system in mouse diabetic nephropathy.
pubmed:affiliation
Laboratory of Anatomy, Department of Biomedical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't