The Experts below are selected from a list of 2193 Experts worldwide ranked by ideXlab platform
Jesus Egido - One of the best experts on this subject based on the ideXlab platform.
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administration of igg fc fragments prevents glomerular injury in experimental Immune Complex Nephritis
Journal of Immunology, 2000Co-Authors: Carmen Gomezguerrero, Natalia Duque, Maria Teresa Casado, Carlos Pastor, Julia Blanco, F Mampaso, Fernando Vivanco, Jesus EgidoAbstract:Most human Nephritis is due to glomerular deposition and/or formation of Immune Complexes (IC). In cultured mesangial cells, Fc receptor stimulation induces proliferation, matrix synthesis, and release of several mediators implicated in the initiation and progression of glomerular injury. Since Ig Fc fragments in vitro modified these phenomena, we studied the effects of systemic administration of IgG Fc fragments on the evolution of experimental IC Nephritis. Fc fragment injection (1 mg/day i.p.) to rats with ongoing Nephritis (proteinuria 20–50 mg/24 h vs 9 ± 0.2 mg/24 h in controls) markedly ameliorates proteinuria, renal function, and morphological renal lesions. This was accompanied by a reduction in the renal synthesis of chemokines (monocyte chemoattractant protein-1, IFN-inducible protein-10, and cytokine-induced neutrophil chemoattractant-1), matrix proteins, and growth factors (platelet-derived growth factor, and TGF-β), and in the activity of transcription factors. The treatment did not affect the glomerular deposition of IgG IC and complement C1q. In contrast, a decrease in the renal expression and production of C3 was observed without changes in serum complement levels. In vitro, very low complement consumption and no C3b covalent interaction were observed with Fc fragments, confirming that they did not modify systemic complement activity. These results indicate that the administration of Fc fragments prevents the development of glomerular damage in an aggressive model of proliferative glomeruloNephritis through mechanisms involving a reduced local generation of complement, chemokines and growth factors. Modulation of IC-mesangial cell interaction by Fc fragment administration could represent a new approach to the treatment of severe Immune Nephritis.
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angiotensin ii participates in mononuclear cell recruitment in experimental Immune Complex Nephritis through nuclear factor κb activation and monocyte chemoattractant protein 1 synthesis
Journal of Immunology, 1998Co-Authors: Marta Ruizortega, C Bustos, Miguel Angel Hernandezpresa, Oscar Lorenzo, Juan Jose Plaza, Jesus EgidoAbstract: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-α. Since NF-κB is involved in the regulation of MCP-1 gene, we explored whether the effects of AngII were mediated through NF-κB activation. Untreated nephritic rats showed increased renal NF-κB activity (3.5-fold) that decreased in response to ACE inhibition. In mesangial cells, AngII activated NF-κB (4.3-fold), and the NF-κB inhibitor pyrrolidine dithiocarbamate abolished the AngII-induced NF-κB activation and MCP-1 gene expression. Our results suggest that AngII could participate in the recruitment of mononuclear cells through NF-κB 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.
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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
Journal of Immunology, 1998Co-Authors: Marta Ruizortega, C Bustos, Miguel Angel Hernandezpresa, Oscar Lorenzo, Juan Jose Plaza, Jesus EgidoAbstract: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.
Marta Ruizortega - One of the best experts on this subject based on the ideXlab platform.
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angiotensin ii participates in mononuclear cell recruitment in experimental Immune Complex Nephritis through nuclear factor κb activation and monocyte chemoattractant protein 1 synthesis
Journal of Immunology, 1998Co-Authors: Marta Ruizortega, C Bustos, Miguel Angel Hernandezpresa, Oscar Lorenzo, Juan Jose Plaza, Jesus EgidoAbstract: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-α. Since NF-κB is involved in the regulation of MCP-1 gene, we explored whether the effects of AngII were mediated through NF-κB activation. Untreated nephritic rats showed increased renal NF-κB activity (3.5-fold) that decreased in response to ACE inhibition. In mesangial cells, AngII activated NF-κB (4.3-fold), and the NF-κB inhibitor pyrrolidine dithiocarbamate abolished the AngII-induced NF-κB activation and MCP-1 gene expression. Our results suggest that AngII could participate in the recruitment of mononuclear cells through NF-κB 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.
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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
Journal of Immunology, 1998Co-Authors: Marta Ruizortega, C Bustos, Miguel Angel Hernandezpresa, Oscar Lorenzo, Juan Jose Plaza, Jesus EgidoAbstract: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.
C Bustos - One of the best experts on this subject based on the ideXlab platform.
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angiotensin ii participates in mononuclear cell recruitment in experimental Immune Complex Nephritis through nuclear factor κb activation and monocyte chemoattractant protein 1 synthesis
Journal of Immunology, 1998Co-Authors: Marta Ruizortega, C Bustos, Miguel Angel Hernandezpresa, Oscar Lorenzo, Juan Jose Plaza, Jesus EgidoAbstract: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-α. Since NF-κB is involved in the regulation of MCP-1 gene, we explored whether the effects of AngII were mediated through NF-κB activation. Untreated nephritic rats showed increased renal NF-κB activity (3.5-fold) that decreased in response to ACE inhibition. In mesangial cells, AngII activated NF-κB (4.3-fold), and the NF-κB inhibitor pyrrolidine dithiocarbamate abolished the AngII-induced NF-κB activation and MCP-1 gene expression. Our results suggest that AngII could participate in the recruitment of mononuclear cells through NF-κB 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.
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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
Journal of Immunology, 1998Co-Authors: Marta Ruizortega, C Bustos, Miguel Angel Hernandezpresa, Oscar Lorenzo, Juan Jose Plaza, Jesus EgidoAbstract: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.
Juan Jose Plaza - One of the best experts on this subject based on the ideXlab platform.
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angiotensin ii participates in mononuclear cell recruitment in experimental Immune Complex Nephritis through nuclear factor κb activation and monocyte chemoattractant protein 1 synthesis
Journal of Immunology, 1998Co-Authors: Marta Ruizortega, C Bustos, Miguel Angel Hernandezpresa, Oscar Lorenzo, Juan Jose Plaza, Jesus EgidoAbstract: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-α. Since NF-κB is involved in the regulation of MCP-1 gene, we explored whether the effects of AngII were mediated through NF-κB activation. Untreated nephritic rats showed increased renal NF-κB activity (3.5-fold) that decreased in response to ACE inhibition. In mesangial cells, AngII activated NF-κB (4.3-fold), and the NF-κB inhibitor pyrrolidine dithiocarbamate abolished the AngII-induced NF-κB activation and MCP-1 gene expression. Our results suggest that AngII could participate in the recruitment of mononuclear cells through NF-κB 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.
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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
Journal of Immunology, 1998Co-Authors: Marta Ruizortega, C Bustos, Miguel Angel Hernandezpresa, Oscar Lorenzo, Juan Jose Plaza, Jesus EgidoAbstract: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.
Oscar Lorenzo - One of the best experts on this subject based on the ideXlab platform.
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angiotensin ii participates in mononuclear cell recruitment in experimental Immune Complex Nephritis through nuclear factor κb activation and monocyte chemoattractant protein 1 synthesis
Journal of Immunology, 1998Co-Authors: Marta Ruizortega, C Bustos, Miguel Angel Hernandezpresa, Oscar Lorenzo, Juan Jose Plaza, Jesus EgidoAbstract: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-α. Since NF-κB is involved in the regulation of MCP-1 gene, we explored whether the effects of AngII were mediated through NF-κB activation. Untreated nephritic rats showed increased renal NF-κB activity (3.5-fold) that decreased in response to ACE inhibition. In mesangial cells, AngII activated NF-κB (4.3-fold), and the NF-κB inhibitor pyrrolidine dithiocarbamate abolished the AngII-induced NF-κB activation and MCP-1 gene expression. Our results suggest that AngII could participate in the recruitment of mononuclear cells through NF-κB 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.
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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
Journal of Immunology, 1998Co-Authors: Marta Ruizortega, C Bustos, Miguel Angel Hernandezpresa, Oscar Lorenzo, Juan Jose Plaza, Jesus EgidoAbstract: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.
