Tobacco smoke cooperates with interleukin-1ß to alter ß-catenin trafficking in vascular endothelium resulting in increased permeability and induction of cyclooxygenase-2 expression in vitro and in vivo Silvia S. Barbieri * ,† and Babette B. Weksler * ,1 * Division of Hematology-Medical Oncology, Weill Medical College of Cornell University, New York, New York, USA; and † Department of Pharmacological Sciences, University of Milan, Milan, Italy 1 Correspondence: Division of Hematology-Medical Oncology, Weill Medical College of Cornell University, 1300 York Ave., 10021 New York, NY, USA. E-mail: babette@med.cornell.edu Cigarette smoking affects all phases of atherosclerosis from endothelial dysfunction to acute occlusive clinical events. We explored activation by exposure to tobacco smoke of two genes, ß-catenin and COX-2, that play key roles in inflammation and vascular remodeling events. Using both in vivo and in vitro smoke exposure, we determined that tobacco smoke (TS) induced nuclear ß-catenin accumulation and COX-2 expression and activity and moreover interacted with IL-1ß to enhance these effects. Exposure of cardiac endothelial cells to tobacco smoke plus IL-1ß (TS/IL-1ß) enhanced permeability of endothelial monolayers and disrupted membrane VE-cadherin/ß-catenin complexes, decreased ß-catenin phosphorylation, and increased phosphorylation of GSK-3ß, Akt, and EGFR. Transfection of endothelial cells with ß-catenin-directed small interferring RNA (siRNA) suppressed TS/IL-1ß-mediated effects on COX-2 modulation. Inhibitors of EGFR and phosphatidylinositol-3-kinase also abolished both the TS/IL-1ß-mediated modulation of the Akt/GSK-3ß/ß-catenin pathway and enhancement of COX-2 expression. Moreover, increased levels of Akt and GSK-3ß phosphorylation, nuclear ß-catenin accumulation, COX-2 expression, and IL-1ß were observed in cardiovascular tissue of ApoE –/– mice exposed to cigarette smoke daily for 2 wk. Our results suggest a novel mechanism by which cigarette smoking can induce proinflammatory and proatherosclerotic effects in vascular tissue.—Barbieri, S. S., Weksler, B. B. Tobacco smoke cooperates with interleukin-1ß to alter ß-catenin trafficking in vascular endothelium resulting in increased permeability and induction of cyclooxygenase-2 expression in vitro and in vivo . Key Words: endothelial cells • inflammation • signal transduction
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Tobacco smoke cooperates with interleukin-1ß to alter ß-catenin trafficking in vascular endothelium resulting in increased permeability and induction of cyclooxygenase-2 expression in vitro and in vivo
Barbieri, Silvia S.; Weksler, Babette B.
Follow The FASEB Journal
, Volume 21 (8): 1831
Fed of American Socs for Experimental Biology – Jun 1, 2007
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