| Wu CH, Chang CH, Lin HC, Chen CM, Lin CH, Lee HM |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=None ------>paper_class3=1 ------>paper_class2=1 ------>vol=66 ------>confirm_bywho=soulchin ------>insert_bywho=chwu ------>Jurnal_Rank=None ------>authors4_c=None ------>comm_author= ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2=212 ------>medlineContent= ------>unit=E0110 ------>insert_date=20030507 ------>iam=1 ------>update_date= ------>author=??? ------>change_event=4 ------>ISSN=None ------>authors_c=None ------>score=500 ------>journal_name=Biochemical Pharmacology ------>paper_name=Role of Protein Kinase C in BSA-AGE-Mediated inducible Nitric Oxide Synthase Expression in RAW 264.7 Macrophages ------>confirm_date=20050625 ------>tch_id=071004 ------>pmid=12826263 ------>page1=203 ------>fullAbstract=In the present study, the roles of protein kinase C (PKC) in BSA-derived advanced glycosylation end products (BSA-AGEs)-induced nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression were investigated. Treatment of RAW 264.7 cells with BSA-AGEs caused dose- and time-dependent increases in NO release and iNOS expression in RAW 264.7 cells, whereas BSA alone had no effect on iNOS induction. The tyrosine kinase inhibitor (genistein), the phosphatidylinositol-specific phospholipase C inhibitor (U-73122), the phosphatidylcholine-specific phospholipase C inhibitor (D-609), and the PKC inhibitors (staurosporine, Ro 31-8220, and Go 6976) all inhibited BSA-AGE-induced NO release and iNOS expression in RAW 264.7 cells. Stimulation of RAW 264.7 cells with BSA-AGEs resulted in the formation of inositol monophosphate; the response was attenuated by U-73122 and genistein. BSA-AGEs stimulated PKC-alpha, -betaI, -delta, and -eta but not -zeta translocation from the cytosol to the membrane. However, incubation of RAW 264.7 cells with BSA-AGEs increased phosphorylation of PKC-zeta at threonine-410, which reflects activation of PKC-zeta, indicating the possible involvement of these PKC isoforms in AGE-mediated effects. Pretreatment of RAW 264.7 cells with U-73122, D-609, and genistein reduced the AGE-stimulated translocation of PKC-alpha, -betaI, -delta, and -eta and activation of PKC-zeta. Taken together, these data suggest that BSA-AGEs might activate PKC and subsequently induce iNOS expression and NO release. ------>tmu_sno=None ------>sno=7232 ------>authors2= ------>authors3= ------>authors4= ------>authors5= ------>authors6= ------>authors6_c=None ------>authors=Wu CH, Chang CH, Lin HC, Chen CM, Lin CH, Lee HM ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=Role of protein kinase C in BSA-AGE-mediated inducible nitric oxide synthase expression in RAW 264.7 macrophages. ------>language=2 ------>check_flag= ------>submit_date= ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho= ------>publish_year=2003 ------>submit_flag= ------>publish_month=None |