| Lin CC |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=2.477 ------>paper_class3=2 ------>paper_class2=1 ------>vol=560 ------>confirm_bywho=sheujr ------>insert_bywho=aspirin ------>Jurnal_Rank=32.6 ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2=109 ------>medlineContent= ------>unit=E0106 ------>insert_date=20070418 ------>iam=7 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c= ------>score=500 ------>journal_name=Eur. J. Pharmacol. ------>paper_name=Transforming growth factor-beta1 stimulates heme oxygenase-1 expression via the PI3K/Akt and NF-kappaB pathways in human lung epithelial cells. ------>confirm_date=20070508 ------>tch_id=095032 ------>pmid=17307160 ------>page1=101 ------>fullAbstract=A previous report showed that transforming growth factor-beta1 (TGF-beta1) can induce heme oxygenase-1 (HO-1) expression, attenuate cellular injury, and maintain tissue homeostasis. In this study, we investigated the involvement of phosphoinositide-3-OH-kinase (PI3K)/Akt and the nuclear factor-kappaB (NF-kappaB) signaling pathway in TGF-beta1-induced HO-1 expression in human lung epithelial cells (A549). Treatment of A549 cells with TGF-beta1 caused HO-1 to be expressed in a concentration- and time-dependent manner. Treatment of A549 cells with LY 294002 (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one, a PI3K inhibitor), an Akt inhibitor, and the dominant negative mutant of Akt (Akt DN) inhibited TGF-beta1-induced HO-1 expression and HO-1-luciferase activity. Stimulation of cells with TGF-beta1 caused an increase in Akt phosphorylation in a time-dependent manner, which was inhibited by wortmannin and LY 294002 (PI3K inhibitors). In addition, treatment of A549 cells with Bay 117082 ((E)-3-[4-methylphenylsulfonyl]-2-propenenitrile, an IkappaB phosphorylation inhibitor), pyrrolidine dithiocarbamate (PDTC, an NF-kappaB inhibitor), and the dominant negative mutant of IkappaBalpha (IkappaBalphaM) inhibited TGF-beta1-induced HO-1 expression and HO-1-luciferase activity. Treatment of A549 cells with TGF-beta1-induced IkappaB kinase alpha/beta (IKKalpha/beta) phosphorylation, IkappaBalpha phosphorylation, IkappaBalpha degradation, p65 Ser536 phosphorylation, and kappaB-luciferase activity. The TGF-beta1-mediated increases in IKKalpha/beta phosphorylation, p65 Ser536 phosphorylation, and kappaB-luciferase activity were inhibited by LY 294002, an Akt inhibitor, and Akt DN. Taken together, these results suggest that the PI3K/Akt dependent IKKalpha/beta/NF-kappaB signaling pathway plays an important role in TGF-beta1-induced HO-1 expression in A549 cells. ------>tmu_sno=None ------>sno=15100 ------>authors2=Chiang LL ------>authors3=Lin CH ------>authors4=Shih CH ------>authors5=Liao YT ------>authors6=Hsu MJ, Chen BC ------>authors6_c= ------>authors=Lin CC ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Transforming growth factor-beta1 stimulates heme oxygenase-1 expression via the PI3K/Akt and NF-kappaB pathways in human lung epithelial cells. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2007 ------>submit_flag=None ------>publish_month=1 |