title: 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.
abstract: BACKGROUND
  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.
  
  
  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.
authors.affiliation: Cellular Biology in Renal Diseases Laboratory, IIS-Fundación Jiménez Díaz Universidad Autónoma Madrid, Spain.
authors.forename: Matilde
authors.initials: M
authors.lastname: Alique
authors.affiliation: Cellular Biology in Renal Diseases Laboratory, IIS-Fundación Jiménez Díaz Universidad Autónoma Madrid, Spain.
authors.forename: Elsa
authors.initials: E
authors.lastname: Sánchez-López
authors.affiliation: Cellular Biology in Renal Diseases Laboratory, IIS-Fundación Jiménez Díaz Universidad Autónoma Madrid, Spain.
authors.forename: Sandra
authors.initials: S
authors.lastname: Rayego-Mateos
authors.affiliation: Renal Research Laboratory, IIS-Fundación Jiménez Díaz Universidad Autónoma Madrid, Spain.
authors.forename: Jesús
authors.initials: J
authors.lastname: Egido
authors.affiliation: Dialysis Unit, IIS-Fundación Jiménez Díaz Universidad Autónoma Madrid, Spain.
authors.forename: Alberto
authors.initials: A
authors.lastname: Ortiz
authors.affiliation: Cellular Biology in Renal Diseases Laboratory, IIS-Fundación Jiménez Díaz Universidad Autónoma Madrid, Spain mruizo@fjd.es.
authors.forename: Marta
authors.initials: M
authors.lastname: Ruiz-Ortega
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D018925:Chemokines / Q000096:biosynthesis / Q000235:genetics; D007249:Inflammation / Q000139:chemically induced* / Q000473:pathology; D053583:Interleukin-1beta / Q000633:toxicity*; D007678:Kidney Glomerulus / Q000166:cytology / Q000187:drug effects; D050527:Mesangial Cells / Q000187:drug effects*; D016328:NF-kappa B / Q000096:biosynthesis / Q000187:drug effects*; D010766:Phosphorylation; D061251:Primary Cell Culture; D051381:Rats; D044140:Receptor, Angiotensin, Type 1 / Q000187:drug effects*
chemical_list: D018925:Chemokines; D053583:Interleukin-1beta; D016328:NF-kappa B; D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II
keywords: Angiotensin II; chemokine; cytokines; kinases; mesangial cells; transcription factors