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The NF-κB family member RelB regulates microRNA miR-146a to suppress cigarette smoke-induced COX-2 protein expression in lung fibroblasts.
In this study we tested whether RelB attenuation of cigarette smoke-induced COX-2 protein is due to miR-146a. Utilizing pulmonary fibroblasts deficient in RelB expression, together with siRNA knock-down of RelB, we show the essential role of RelB in diminishing smoke-induced COX-2 protein expression despite robust activation of the canonical NF-κB pathway and subsequent induction of Cox-2 mRNA. RelB did not regulate COX-2 protein expression at the level of mRNA stability. Basal levels of miR-146a were significantly lower in Relb-deficient cells and cigarette smoke increased miR-146a expression only in Relb-expressing cell...
Source: Toxicology Letters - January 25, 2014 Category: Toxicology Authors: Zago M, de Souza AR, Hecht E, Rousseau S, Hamid Q, Eidelman DH, Baglole CJ Tags: Toxicol Lett Source Type: research

Smad3 mediates cigarette smoke extract (CSE) induction of VEGF release by human fetal lung fibroblasts.
Abstract Cigarette smoke is the major cause of chronic obstructive pulmonary disease (COPD), yet pathogenic mechanisms are not fully understood. Vascular endothelial growth factor (VEGF) is one of the major regulators of endothelial cell survival and is believed to play a role in the pathogenesis of COPD. Fibroblasts are a significant source of VEGF in the lungs; however the effect of cigarette smoke exposure on VEGF release by fibroblasts is not fully understood. We hypothesized that cigarette smoke-induced disturbed VEGF release by human lung fibroblasts is a potential pathogenic mechanism that could contribute ...
Source: Toxicology Letters - April 22, 2013 Category: Toxicology Authors: Farid M, Kanaji N, Nakanishi M, Gunji Y, Michalski J, Iwasawa S, Ikari J, Wang X, Basma H, Nelson AJ, Liu X, Rennard SI Tags: Toxicol Lett Source Type: research