Linked Life Data

15153562

Source:http://linkedlifedata.com/resource/pubmed/id/15153562

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2004-5-21
pubmed:abstractText
Inflammatory cell infiltration plays a key role in the onset and progression of renal injury. The NF-kappaB participates in the inflammatory response, regulating many proinflammatory genes. Angiotensin II (Ang II), via AT(1) and AT(2) receptors, activates NF-kappaB. Although the contribution of Ang II to kidney damage progression is already established, the receptor subtype involved in the inflammatory cell recruitment is not clear. For investigating this issue, the unilateral ureteral obstruction (UUO) model was used in mice, blocking Ang II production/receptors and NF-kappaB pathway. Two days after UUO, obstructed kidneys of wild-type mice presented a marked interstitial inflammatory cell infiltration and increased NF-kappaB activity. Treatment with AT(1) or AT(2) antagonists partially decreased NF-kappaB activation, whereas only the AT(2) blockade diminished monocyte infiltration. Obstructed kidneys of AT(1)-knockout mice showed interstitial monocyte infiltration and NF-kappaB activation; both processes were abolished by an AT(2) antagonist, suggesting AT(2)/NF-kappaB involvement in monocyte recruitment. In wild-type mice, only angiotensin-converting enzyme inhibition or combined therapy with AT(1) plus AT(2) antagonists blocked monocyte infiltration, NF-kappaB activation, and upregulation of NF-kappaB-related proinflammatory genes. Therefore, AT(1) and AT(2) blockade is necessary to arrest completely the inflammatory process. Treatment with two different NF-kappaB inhibitors, pirrolidin-dithiocarbamate and parthenolide, diminished monocyte infiltration and gene overexpression. These data show that Ang II, via AT(1) and AT(2) receptors and NF-kappaB pathway, participates in the regulation of renal monocyte recruitment and may provide a rationale to investigate further the role of AT(2) in human kidney diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1514-29
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15153562-Angiotensin II, pubmed-meshheading:15153562-Animals, pubmed-meshheading:15153562-Disease Progression, pubmed-meshheading:15153562-Gene Expression Regulation, pubmed-meshheading:15153562-Genotype, pubmed-meshheading:15153562-Immunohistochemistry, pubmed-meshheading:15153562-Inflammation, pubmed-meshheading:15153562-Kidney, pubmed-meshheading:15153562-Kidney Diseases, pubmed-meshheading:15153562-Mice, pubmed-meshheading:15153562-Mice, Inbred C57BL, pubmed-meshheading:15153562-Mice, Knockout, pubmed-meshheading:15153562-NF-kappa B, pubmed-meshheading:15153562-RNA, pubmed-meshheading:15153562-Receptor, Angiotensin, Type 1, pubmed-meshheading:15153562-Receptor, Angiotensin, Type 2, pubmed-meshheading:15153562-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:15153562-Time Factors, pubmed-meshheading:15153562-Up-Regulation, pubmed-meshheading:15153562-Ureteral Obstruction
pubmed:year
2004
pubmed:articleTitle
Angiotensin II, via AT1 and AT2 receptors and NF-kappaB pathway, regulates the inflammatory response in unilateral ureteral obstruction.
pubmed:affiliation
Vascular and Renal Research Laboratory, Fundación Jiménez Díaz, Universidad Autónoma, Avda. Reyes Católicos 2, 28040 Madrid, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't