| Cheng YW |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=3.249 ------>paper_class3=2 ------>paper_class2=1 ------>vol=28 ------>confirm_bywho=amel ------>insert_bywho=ywcheng ------>Jurnal_Rank=20.0 ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2=178 ------>medlineContent= ------>unit=G0100 ------>insert_date=20090708 ------>iam=1 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c= ------>score=421 ------>journal_name=Toxicology Letters ------>paper_name=Cholesterol-3-beta,5-alpha,6-beta-triol induced PI3K-Akt-eNOS-dependent cyclooxygenase-2 expression in endothelial cells ------>confirm_date=20091016 ------>tch_id=089070 ------>pmid=19616084 ------>page1=172 ------>fullAbstract=Oxidized cholesterols belong to a subgroup of oxLDLs which play major roles in atherosclerosis. In order to investigate the contribution of oxysterols from oxLDLs in atherosclerosis, cholesterol-3-beta, 5-alpha, 6-beta-triol (alpha-Triol) was studied in human umbilical vein endothelial cells. We found that alpha-Triol concentration- and time-dependently enhanced COX-2 protein expression and mRNA production followed by PGE(2) generation in human umbilical vein endothelial cells. In addition, alpha-Triol upregulated peNOS(1177) protein phosphorylation and concentration-dependently increased nitric oxide production. eNOS(1177) phosphorylation was abrogated by the PI3K inhibitor, LY294002. In studying the mechanisms involved in alpha-Triol-induced COX-2/PGE(2) production, inhibitors of NOS, PI3K, p38, and NF-kappaB, effectively attenuated COX-2 protein induction and mRNA expression, suggesting that the PI(3)K-Akt-eNOS pathway, p38MAPK, and NF-kappaB are involved in alpha-Triol-induced COX-2 expression, and following increases in p38 and Akt phosphorylation, the concentration-dependent inhibition of COX-2 protein expression by L-NAME further suggested their involvement at the translation level. We concluded that alpha-Triol increases COX-2 mRNA and protein expression via coordination with the PI(3)K-Akt-eNOS pathway and NF-kappaB. Moreover, COX-2 gene expression might be regulated by activated p38 MAPK in another unknown regulation pathway. Our findings also suggested that alpha-Triol might contribute to the effect of induced atherosclerosis in humans through COX-2 production in endothelial cells. ------>tmu_sno=None ------>sno=22020 ------>authors2=Liao PL ------>authors3=Li CH ------>authors4=Lo YL ------>authors5=Kang JJ ------>authors6= ------>authors6_c= ------>authors=Cheng YW ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Cholesterol-3-beta, 5-alpha, 6-beta-triol induced PI(3)K-Akt-eNOS-dependent cyclooxygenase-2 expression in endothelial cells. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no=192(2) ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2009 ------>submit_flag=None ------>publish_month=7 |