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Blood, 15 September 2007, Vol. 110, No. 6, pp. 1895-1902.
Prepublished online as a Blood First Edition Paper on June 26, 2007; DOI 10.1182/blood-2007-01-070607.
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Submitted January 26, 2007
Accepted June 6, 2007
A critical role for TNF in the selective attachment of mononuclear leukocytes to angiotensin-II-stimulated arterioles
Teresa Mateo, Yafa Naim Abu Nabah, Mercedes Losada, Rossana Estelles, Chantal Company, Begona Bedrina, Jose Miguel Cerda-Nicolas, Stephen Poole, Peter J Jose, Julio Cortijo, Esteban J Morcillo, and Maria-Jesus Sanz*
Department of Pharmacology, Faculty of Medicine, University of Valencia, Valencia, Spain
Department of Pathology, Faculty of Medicine, University of Valencia, Valencia, Spain
Division of endocrinology, National Institute for Biological Standards and Control, South Mimms, United Kingdom
Research Foundation, University General Hospital Consortium, Valencia, Spain
Clinical Pharmacology Unit, University Clinical Hospital, Valencia, Spain
Ciber CB06/06/0027 "Respiratory Diseases", Carlos III Health Institute, Spanish Ministry of Health, Valencia, Spain
* Corresponding author; email: maria.j.sanz{at}uv.es.
Angiotensin II (Ang-II) exerts inflammatory activity and is involved in different cardiovascular disorders. This study has evaluated the involvement of TNF in the leukocyte accumulation elicited by Ang-II. Ang-II (1 nmol/L, i.p., in rats) induced TNF release at 1h followed by neutrophil and mononuclear cell recruitment. The administration of an anti-rat TNF antiserum had no effect on Ang-II-induced neutrophil accumulation but inhibited the infiltration of mononuclear cells and reduced CC chemokine content in the peritoneal exudate. Pretreatment with either an anti-TNF or an anti-IL-4 antiserum decreased Ang-II-induced arteriolar mononuclear leukocyte adhesion by 68 and 60% respectively in the rat mesenteric microcirculation. While no expression of TNF was found in the post-capillary venules of Ang-II injected animals, this cytokine was clearly up-regulated in the arterioles. Stimulation of HUAECs or isolated human mononuclear cells with 1 µmol/L Ang-II caused increased TNF mRNA expression and protein. Neutralization of TNF activity reduced Ang-II-induced MCP-1, MCP-3 and RANTES release from HUAECs and MIP-1 from blood cells. In conclusion, the selective mononuclear leukocyte adhesion to Ang-II stimulated arterioles is largely mediated by TNF in cooperation with constitutive IL-4. Therefore, neutralization of TNF activity may help to prevent mononuclear cell infiltration and the progression of the atherogenic process.
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