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Updated: Jun 12, 2026
Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System
Published on: October 22, 2020
Cigarette smoke extract induces HO-1 expression in mouse cerebral vascular endothelial cells: involvement of
Ruey-Horng Shih1, I-Ta Lee, Hsi-Lung Hsieh
1Department of Physiology and Pharmacology, Chang Gung University, Tao-Yuan, Taiwan.
Abstract:
Several chemicals present in cigarette smoke (CS) have been reported to induce heme oxygenase-1 (HO-1) expression, which represents a prime defense mechanism in protecting the cells from stress-dependent adverse effects on peripheral vascular system. However, the effects of cigarette smoke extract (CSE) on HO-1 induction and the mechanisms underlying CSE-induced HO-1 expression in brain vessels are not completely understood. Here, we used a mouse brain endothelial cell culture (bEnd.3) to investigate the effect of CSE on HO-1 induction and the mechanisms underlying CSE-induced HO-1 expression in cerebral vessels. We demonstrated that sublethal concentrations of CSE (30 µg/ml) induced submaximal HO-1 expression in bEnd.3 cells. NADPH oxidase-dependent ROS generation played a key role in CSE-induced HO-1 expression. CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was observed by pretreatment with the respective pharmacological inhibitors or transfection with PDGFR shRNA. CSE activated NADPH oxidase through c-Src in bEnd.3 cells. Taken together, these results suggested that, in bEnd.3 cells, CSE-induced HO-1 expression was mediated through PDGFR/JAK2/STAT3 cascade, which was regulated by c-Src or c-Src activated-NADPH oxidase/ROS.
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