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Am J Physiol Lung Cell Mol Physiol (October 13, 2006). doi:10.1152/ajplung.00308.2006
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Submitted on August 10, 2006
Accepted on October 7, 2006

Sirtuin regulates cigarette smoke induced pro-inflammatory mediators release via RelA/p65 NF-{kappa}B in macrophages in vitro and in rat lungs in vivo

Se-Ran Yang1, Jessica Wright1, Mark Bauter1, Kathryn Seweryniak1, Aruna Kode1, and Irfan Rahman1*

1 Environmental Medicine, University of Rochester, Rochester, New York, United States

* To whom correspondence should be addressed. E-mail: irfan_rahman{at}urmc.rochester.edu.

The Silent information regulator2 (Sir2) family of proteins (sirtuins or SIRT) which belong to class III histone/protein deacetylases, have been implicated in calorie restriction, aging and inflammation. We hypothesized that cigarette smoke-mediated pro-inflammatory cytokine release is regulated by SIRT1 by its interaction with NF-{kappa}B in the monocyte-macrophage cell line (MonoMac6) and in inflammatory cells of rat lungs. Cigarette smoke extract (CSE) exposure to MonoMac6 cells caused dose- and time-dependent decrease in SIRT1 activity and levels, that was concomitant to increased NF-{kappa}B-dependent pro-inflammatory mediators release. Similar decrements in SIRT1 were also observed in inflammatory cells in the lungs of rats exposed to cigarette smoke as well as with increased levels of several NF-{kappa}B-dependent pro-inflammatory mediators in bronchoalveolar lavage fluid and in lungs. Sirtinol, an inhibitor of SIRT1, augmented whereas resveratrol, an activator of SIRT1, inhibited CSE-mediated pro-inflammatory cytokine release. CSE-mediated inhibition of SIRT1 was associated with increased NF-{kappa}B levels. Furthermore, we showed that SIRT1 interacts with RelA/p65 subunit of NF-{kappa}B, which was disrupted by cigarette smoke, leading to increased acetylation RelA/p65 in MonoMac6 cells. Thus, our data show that SIRT1 regulates cigarette smoke-mediated pro-inflammatory mediator release via NF-{kappa}B implicating a role of SIRT1 in sustained inflammation and aging of the lungs.




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