Angiotensin II, via angiotensin receptor type 1/nuclear factor-κB activation, causes a synergistic effect on interleukin-1-β-induced inflammatory responses in cultured mesangial cells

Introduction: The nuclear factor-κB (NF-κB) is an important regulator of the inflammatory response. Angiotensin II (Ang II) activates the NF-κB pathway linked to renal inflammation. Although both AT1 and AT2 receptors are involved in Ang II-mediated NF-κB activation, the biological processes mediate...

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Published in:Journal of the renin-angiotensin-aldosterone system 2015-03, Vol.16 (1), p.23-32
Main Authors: Alique, Matilde, Sánchez-López, Elsa, Rayego-Mateos, Sandra, Egido, Jesús, Ortiz, Alberto, Ruiz-Ortega, Marta
Format: Article
Language:English
Subjects:
Angiotensin II - metabolism
Animals
Chemokines - biosynthesis
Chemokines - genetics
Inflammation - chemically induced
Inflammation - pathology
Interleukin-1beta - toxicity
Kidney Glomerulus - cytology
Kidney Glomerulus - drug effects
Mesangial Cells - drug effects
NF-kappa B - biosynthesis
NF-kappa B - drug effects
Phosphorylation
Primary Cell Culture
Rats
Receptor, Angiotensin, Type 1 - drug effects
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Summary:Introduction: The nuclear factor-κB (NF-κB) is an important regulator of the inflammatory response. Angiotensin II (Ang II) activates the NF-κB pathway linked to renal inflammation. Although both AT1 and AT2 receptors are involved in Ang II-mediated NF-κB activation, the biological processes mediated by each receptor are not fully characterized. Interleukin-1β (IL-1β) is an important macrophage-derived cytokine that regulates immune and inflammatory processes, activating intracellular pathways shared with Ang II, including the NF-κB. Materials and methods: In vitro studies were done in primary cultured rat mesangial cells. NF-κB pathway was evaluated by phosphorylated levels of p65/IκB and DNA binding activity. The Ang II receptor subtype was determined by pretreatment with AT1 and AT2 antagonists. Results: In mesangial cells the simultaneous presence of Ang II and IL-1β caused a synergistic activation of the NF-κB pathway and a marked upregulation of proinflammatory factors under NF-κB control, including monocyte chemoattractant protein-1. The AT1, but not AT2, antagonist abolished the synergistic effect on NF-κB activation and proinflammatory genes caused by coincubation of Ang II and IL-1β. Conclusions: These data indicates that Ang II, via AT1/NF-κB pathway activation, cooperates with IL-β to increase the inflammatory response in mesangial cells.
ISSN:1470-3203
1752-8976
DOI:10.1177/1470320314551564