title: Nicotine induces cyclooxygenase-2 and prostaglandin E(2) expression in human umbilical vein endothelial cells.
abstract: Nicotine is a major component of cigarette smoking which may be involved in the progress of atherogenesis. In order to explain the mechanism of nicotine-induced endothelium dysfunction, we investigated the effects of nicotine on cyclooxygenase-2 (COX-2) and intercellular adhesion molecule-1 (ICAM-1) expression in human umbilical vein endothelial cells (HUVECs). Nicotine treatment increased the expressions of COX-2 at mRNA and protein level in a dose-dependent manner, following prostaglandin E(2) (PGE(2)) release enhancement. Pyrrolidine dithiocarbamate (PDTC, NF-kappaB inhibitor) and alpha-Bungarotoxin (alpha-Btx, nicotinic acetylcholine receptor antagonist) attenuated the nicotine-induced COX-2 expression and PGE(2) production. Furthermore, nicotine-induced ICAM-1 expression was reduced by NS-398 (selective COX-2 inhibitor). Taken together, the present study demonstrated that nicotine-induced COX-2 expression through NF-kappaB activation which mediated by nicotinic acetylcholine receptor and the induction of COX-2 was related to ICAM-1 expression.
authors.affiliation: School of Life Sciences and Biotechnology, Bio-X Research Center, Key Laboratory for Developmental Genetics and Neuropsychiatric Diseases (Ministry of Education), Shanghai Jiao Tong University, 800 Dongchuan Rd, 200240 Shanghai, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhou
authors.forename: Zhao-Xia
authors.initials: ZX
authors.lastname: Wang
authors.forename: Mao-Ping
authors.initials: MP
authors.lastname: Tang
authors.forename: Chen-Jiang
authors.initials: CJ
authors.lastname: Yao
authors.forename: Wang-Jie
authors.initials: WJ
authors.lastname: Xu
authors.forename: Lian-Yun
authors.initials: LY
authors.lastname: Wang
authors.forename: Zhong-Dong
authors.initials: ZD
authors.lastname: Qiao
mesh_terms: D015153:Blotting, Western; D002467:Cell Nucleus / Q000737:chemistry / Q000378:metabolism; D002478:Cells, Cultured; D051546:Cyclooxygenase 2 / Q000096:biosynthesis*; D015232:Dinoprostone / Q000096:biosynthesis*; D024202:Electrophoretic Mobility Shift Assay; D042783:Endothelial Cells / Q000187:drug effects / Q000201:enzymology* / Q000378:metabolism; D004790:Enzyme Induction / Q000187:drug effects; D005260:Female; D005455:Fluorescent Antibody Technique; D006801:Humans; D007202:Indicators and Reagents; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D009538:Nicotine / Q000494:pharmacology*; D018722:Nicotinic Agonists / Q000494:pharmacology*; D018733:Nicotinic Antagonists / Q000494:pharmacology; D011247:Pregnancy; D011978:Receptors, Nicotinic / Q000187:drug effects; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013268:Stimulation, Chemical; D014471:Umbilical Veins / Q000166:cytology
chemical_list: D007202:Indicators and Reagents; D018722:Nicotinic Agonists; D018733:Nicotinic Antagonists; D011978:Receptors, Nicotinic; D018799:Intercellular Adhesion Molecule-1; D009538:Nicotine; D051546:Cyclooxygenase 2; D015232:Dinoprostone