Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-7-9
pubmed:abstractText
Angiotensin-converting enzyme (ACE) inhibitors reduce macrophage infiltration in several models of renal injury. We approached the hypothesis that angiotensin II (AngII) could be involved in inflammatory cell recruitment during renal damage through the synthesis of monocyte chemoattractant protein-1 (MCP-1). In a model of immune complex nephritis, we observed an up-regulation of renal MCP-1 (mRNA and protein) coincidentally with mononuclear cell infiltration that were markedly reduced by treatment with the ACE inhibitor quinapril. Exposure of cultured rat mesangial cells to AngII increased MCP-1 mRNA expression (2.7-fold) and synthesis (3-fold), similar to that observed with TNF-alpha. Since NF-kappaB is involved in the regulation of MCP-1 gene, we explored whether the effects of AngII were mediated through NF-kappaB activation. Untreated nephritic rats showed increased renal NF-kappaB activity (3.5-fold) that decreased in response to ACE inhibition. In mesangial cells, AngII activated NF-kappaB (4.3-fold), and the NF-kappaB inhibitor pyrrolidine dithiocarbamate abolished the AngII-induced NF-kappaB activation and MCP-1 gene expression. Our results suggest that AngII could participate in the recruitment of mononuclear cells through NF-kappaB activation and MCP-1 expression by renal cells. This could be a novel mechanism that might further explain the beneficial effects of ACE inhibitors in progressive renal diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
161
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
430-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9647253-Administration, Oral, pubmed-meshheading:9647253-Angiotensin II, pubmed-meshheading:9647253-Angiotensin-Converting Enzyme Inhibitors, pubmed-meshheading:9647253-Animals, pubmed-meshheading:9647253-Cell Movement, pubmed-meshheading:9647253-Cells, Cultured, pubmed-meshheading:9647253-Chemokine CCL2, pubmed-meshheading:9647253-Down-Regulation, pubmed-meshheading:9647253-Glomerular Mesangium, pubmed-meshheading:9647253-Glomerulonephritis, pubmed-meshheading:9647253-Immune Complex Diseases, pubmed-meshheading:9647253-Isoquinolines, pubmed-meshheading:9647253-Kidney Glomerulus, pubmed-meshheading:9647253-Leukocytes, Mononuclear, pubmed-meshheading:9647253-NF-kappa B, pubmed-meshheading:9647253-RNA, Messenger, pubmed-meshheading:9647253-Rats, pubmed-meshheading:9647253-Rats, Wistar, pubmed-meshheading:9647253-Tetrahydroisoquinolines, pubmed-meshheading:9647253-Up-Regulation
pubmed:year
1998
pubmed:articleTitle
Angiotensin II participates in mononuclear cell recruitment in experimental immune complex nephritis through nuclear factor-kappa B activation and monocyte chemoattractant protein-1 synthesis.
pubmed:affiliation
Renal Unit, Fundación Jiménez Díaz, Universidad Autónoma, Madrid, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't