Epidemiological studies demonstrated a relationship between cigarette smoking and cardiovascular disease. Smoke from burned cigarettes produces various oxidative species and free radicals in gas or particle phase. These species cause endothelial dysfunction and inflammation. Adhesion of leukocytes and activation of adhesion molecules (E-selectin, VCAM-1, ICAM-1 ) are present in atherosclerosis.
In this study, CSE-induced surface expression of ICAM-1 and E-selectin in human umbilical vein endothelial cells was investigated. Also, the binding activity of transcription factors (AP-1) was determined by electrophoretic mobility shift assay (EMSA). Results showed that cigarette smoke extracts (CSE) induced AP-1 binding activity. We examined MAPKs (JNK1, ERK1/2) activities by using Western blot assay. Furthermore, CSE-stimulated phosphorylation of ERK1/2 and JNK1 was attenuated by the pretreatment with PD98059 and SP600125 respectively, although CSE-induced expression of ICAM-1 and E-selectin was not attenuated. CSE-induced surface expression of ICAM-1 and E-selectin was attenuated by the pretreatment with F-actin filament inhibitor cytochalasinD.
These results suggested that HUVECs pretreated with F-actin filament inhibitor (cytochalasin D) would effectively inhibit CSE-induced expression of ICAM-1 and E-selectin, Although the ERK1/2, JNK1 and AP-1 activation was enhanced by CSE treatment, the enhanced activation may not be necessary in the expression of the ICAM-1 and E-selectin in HUVECs.
