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
| Autor: | Sandra Rayego-Mateos, Alberto Ortiz, Matilde Alique, Jesús Egido, Elsa Sanchez-Lopez, Marta Ruiz-Ortega |
|---|---|
| Přispěvatelé: | UAM. Departamento de Medicina, Instituto de Investigación Sanitaria Fundación Jiménez Díaz (IIS-FJD) |
| Rok vydání: | 2014 |
| Předmět: |
Chemokine
medicine.medical_specialty Angiotensin receptor Medicine (General) Medicina medicine.medical_treatment Interleukin-1beta Kidney Glomerulus Primary Cell Culture Inflammation Kinases Receptor Angiotensin Type 1 Proinflammatory cytokine Endocrinology R5-920 Mesangial cells Internal medicine Internal Medicine medicine Transcription factors Animals Phosphorylation Receptor Angiotensin II receptor type 1 biology Angiotensin II NF-kappa B Cell biology Rats Cytokine Mesangial Cells cardiovascular system biology.protein Cytokines medicine.symptom Chemokines hormones hormone substitutes and hormone antagonists |
| Zdroj: | Journal of the Renin-Angiotensin-Aldosterone System, Vol 16 (2015) Biblos-e Archivo. Repositorio Institucional de la UAM instname |
| ISSN: | 1752-8976 |
| Popis: | 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 This work was supported by grants from the Instituto de Salud Carlos III (ISCIIIRETIC REDinREN RD06/0016, RD12/0021, PI11/01854), Comunidad de Madrid (Fibroteam S2010/BMD- 2321, S2010/BMD-2378), and Research Institute Queen Sophia (IRSIN). Programa Intensificación Actividad Investigadora (ISCIII/Agencia Laín-Entralgo/CM) to AO. MA and ESL are supported by a ‘Sara Borrell’ postdoctoral contract from Instituto de Salud Carlos III (CD10/00347 and CD09/00066, respectively) |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|