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. (March 2015)

• Record Type: Journal Article
• Authors: Alique, Matilde; Sánchez-López, Elsa; Rayego-Mateos, Sandra; Egido, Jesús; Ortiz, Alberto; Ruiz-Ortega, Marta
• Is Part Of: Journal of the renin-angiotensin-aldosterone system. Volume 16:Number 1(2015:Mar.)
• Page Start: 23
• Page End: 32
• Publication Date: 2015-03
• Subjects: Angiotensin II -- cytokines -- mesangial cells -- transcription factors -- kinases -- chemokine; Renin-angiotensin system -- Periodicals; 616.132
• DOI: 10.1177/1470320314551564
• Languages: English
• ISSNs: 1470-3203

Abstract

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.