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Am J Physiol Cell Physiol (May 18, 2005). doi:10.1152/ajpcell.00045.2005
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Submitted on February 4, 2005
Accepted on May 3, 2005

Novel lipid mediator aspirin-triggered lipoxin A4 induces heme oxygenase-1 on endothelial cells

Vany Nascimento-Silva1, Maria A Arruda1, Christina Barja-Fidalgo1, Christina G Villela1, and Iolanda M Fierro1*

1 Farmacologia e Psicobiologia, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brazil

* To whom correspondence should be addressed. E-mail: iolanda{at}uerj.br.

Lipoxins (LX) and aspirin-triggered LX (ATL) are eicosanoids generated via transcellular biosynthetic routes during inflammation, that elicit distinct anti-inflammatory and proresolution bioactions, including inhibition of leukocyte-mediated injury, stimulation of macrophage clearance of apoptotic neutrophils, repression of proinflammatory cytokines production, and inhibition of cell proliferation and migration. Recently, it was reported that aspirin induces heme-oxygenase-1 (HO-1) expression on endothelial cells (EC) in a COX- independent manner, what confers protection against pro-oxidant insults. However, the underlying mechanisms remain unclear. In this study, we investigated whether an aspirin-triggered lipoxin A4 stable analog, 15-epi-16-(para-fluoro)-phenoxy-lipoxin A4 (ATL-1) was able to induce endothelial HO-1. Western blot analysis showed that ATL-1 increased HO-1 protein expression associated with increased mRNA levels on EC in a time and concentration-dependent fashion. This phenomenon appears to be mediated by the activation of the G-protein-coupled LXA4 receptor since pertussis toxin and Boc-2, a receptor antagonist, treatment significantly inhibited ATL-1-induced HO-1 expression. We demonstrate that treatment of EC with ATL-1 inhibited V-CAM and E-selectin expression induced by TNF-{alpha} or IL-1{beta}. This inhibitory effect of the analog is modulated by HO-1, since it was blocked by SnPPIX, a competitive inhibitor that blocks HO-1 activity. Our results establish that ATL-1 induce HO-1 in human EC, revealing an undescribed mechanism for the anti-inflammatory activity of these lipid mediators.




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