PMID- 9647253
OWN - NLM
STAT- MEDLINE
DCOM- 19980709
LR  - 20181201
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 161
IP  - 1
DP  - 1998 Jul 1
TI  - Angiotensin II participates in mononuclear cell recruitment in experimental 
      immune complex nephritis through nuclear factor-kappa B activation and monocyte 
      chemoattractant protein-1 synthesis.
PG  - 430-9
AB  - 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.
FAU - Ruiz-Ortega, M
AU  - Ruiz-Ortega M
AD  - Renal Unit, Fundacion Jimenez Diaz, Universidad Autonoma, Madrid, Spain.
FAU - Bustos, C
AU  - Bustos C
FAU - Hernandez-Presa, M A
AU  - Hernandez-Presa MA
FAU - Lorenzo, O
AU  - Lorenzo O
FAU - Plaza, J J
AU  - Plaza JJ
FAU - Egido, J
AU  - Egido J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Isoquinolines)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tetrahydroisoquinolines)
RN  - 11128-99-7 (Angiotensin II)
RN  - RJ84Y44811 (Quinapril)
SB  - IM
MH  - Administration, Oral
MH  - Angiotensin II/pharmacology/*physiology
MH  - Angiotensin-Converting Enzyme Inhibitors/administration & dosage
MH  - Animals
MH  - Cell Movement/drug effects/*immunology
MH  - Cells, Cultured
MH  - Chemokine CCL2/antagonists & inhibitors/*biosynthesis/genetics
MH  - Down-Regulation/drug effects/immunology
MH  - Glomerular Mesangium/drug effects/metabolism
MH  - Glomerulonephritis/*immunology/pathology
MH  - Immune Complex Diseases/*immunology/pathology
MH  - Isoquinolines/administration & dosage
MH  - Kidney Glomerulus/pathology
MH  - Leukocytes, Mononuclear/*immunology/pathology
MH  - NF-kappa B/antagonists & inhibitors/*metabolism
MH  - Quinapril
MH  - RNA, Messenger/biosynthesis/drug effects
MH  - Rats
MH  - Rats, Wistar
MH  - *Tetrahydroisoquinolines
MH  - Up-Regulation/drug effects/immunology
EDAT- 1998/07/01 00:00
MHDA- 1998/07/01 00:01
CRDT- 1998/07/01 00:00
PHST- 1998/07/01 00:00 [pubmed]
PHST- 1998/07/01 00:01 [medline]
PHST- 1998/07/01 00:00 [entrez]
PST - ppublish
SO  - J Immunol. 1998 Jul 1;161(1):430-9.