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Rheumatology Advance Access originally published online on May 27, 2007
Rheumatology 2007 46(8):1252-1257; doi:10.1093/rheumatology/kem092
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Angiotensin II protects fibroblast-like synoviocytes from apoptosis via the AT1-NF-{kappa}B pathway

L. Pattacini, B. Casali, L. Boiardi1, N. Pipitone1, L. Albertazzi2 and C. Salvarani1

Laboratorio di Biologia Molecolare, 1Unità Operativa di Reumatologia, 2Laboratorio Analisi Chimico-Cliniche, Arcispedale S. Maria Nuova, Viale Risorgimento, 80, 42100 Reggio Emilia, Italy.

Correspondence to: C. Salvarani, Unità Operativa di Reumatologia, Arcispedale S. Maria Nuova, Viale Risorgimento, 80, 42100 Reggio Emilia, Italy. E-mail: salvarani.carlo{at}asmn.re.it


  Abstract

Objective. To evaluate the effects of angiotensin II (Ang II) treatment on apoptosis of fibroblast-like synoviocytes (FLS) from patients with osteoarthritis (OA) and rheumatoid arthritis (RA).

Methods. AT1 receptor expression was detected by western blotting and flow cytometry. Apoptosis induction was quantified by nucleosome ELISA and by TUNEL; cell proliferation was determined by a bromodeoxyuridine (BrdU) incorporation assay. Silencing of p65 NF-{kappa}B was obtained by using a specific siRNA. Caspase 3 activation was evaluated by a colorimetric assay and its cleavage by western blotting.

Results. AT1 expression resulted comparable in FLS from OA and RA patients. Ang II pre-treatment reduced FLS apoptotic response to serum starvation and nitric oxide (NO) exposure. This protective effect was reverted in the presence of the AT1 receptor antagonist losartan as well as after silencing the expression of NF-{kappa}B. Moreover, FLS treatment with the caspase inhibitor z-VAD-fmk cancelled this Ang II effect on apoptosis. Caspase 3 activation was reduced in presence of Ang II.

Conclusions. Ang II could represent an important mediator involved in FLS expansion, reducing their capacity to undergo apoptosis, through the activation of NF-{kappa}B and the blockage of caspase cascade.

KEY WORDS: Apoptosis, Angiotensin II, Fibroblast-like synoviocytes, NF-{kappa}B, Rheumatoid arthritis, Osteoarthritis

Submitted 1 December 2006; revised version accepted 20 March 2007.
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