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Angiotensin II participates in mononuclear cell recruitment in experimental immune complex nephritis through nuclear factor-kappa B activation and monocyte chemoattractant protein-1 synthesis.
J Immunol. 1998 Jul 01; 161(1):430-9.JI

Abstract

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.

Authors+Show Affiliations

Renal Unit, Fundación Jiménez Díaz, Universidad Autónoma, Madrid, Spain.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9647253

Citation

Ruiz-Ortega, M, et al. "Angiotensin II Participates in Mononuclear Cell Recruitment in Experimental Immune Complex Nephritis Through Nuclear Factor-kappa B Activation and Monocyte Chemoattractant Protein-1 Synthesis." Journal of Immunology (Baltimore, Md. : 1950), vol. 161, no. 1, 1998, pp. 430-9.
Ruiz-Ortega M, Bustos C, Hernández-Presa MA, et al. Angiotensin II participates in mononuclear cell recruitment in experimental immune complex nephritis through nuclear factor-kappa B activation and monocyte chemoattractant protein-1 synthesis. J Immunol. 1998;161(1):430-9.
Ruiz-Ortega, M., Bustos, C., Hernández-Presa, M. A., Lorenzo, O., Plaza, J. J., & Egido, J. (1998). Angiotensin II participates in mononuclear cell recruitment in experimental immune complex nephritis through nuclear factor-kappa B activation and monocyte chemoattractant protein-1 synthesis. Journal of Immunology (Baltimore, Md. : 1950), 161(1), 430-9.
Ruiz-Ortega M, et al. Angiotensin II Participates in Mononuclear Cell Recruitment in Experimental Immune Complex Nephritis Through Nuclear Factor-kappa B Activation and Monocyte Chemoattractant Protein-1 Synthesis. J Immunol. 1998 Jul 1;161(1):430-9. PubMed PMID: 9647253.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Angiotensin II participates in mononuclear cell recruitment in experimental immune complex nephritis through nuclear factor-kappa B activation and monocyte chemoattractant protein-1 synthesis. AU - Ruiz-Ortega,M, AU - Bustos,C, AU - Hernández-Presa,M A, AU - Lorenzo,O, AU - Plaza,J J, AU - Egido,J, PY - 1998/7/1/pubmed PY - 1998/7/1/medline PY - 1998/7/1/entrez SP - 430 EP - 9 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 161 IS - 1 N2 - 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. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/9647253/Angiotensin_II_participates_in_mononuclear_cell_recruitment_in_experimental_immune_complex_nephritis_through_nuclear_factor_kappa_B_activation_and_monocyte_chemoattractant_protein_1_synthesis_ L2 - http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=9647253 DB - PRIME DP - Unbound Medicine ER -