| Liu DZ |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=6.900 ------>paper_class3=2 ------>paper_class2=1 ------>vol=73 ------>confirm_bywho=hsuan ------>insert_bywho=wbzhong ------>Jurnal_Rank=11.1 ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=17 ------>paper_class2Letter=None ------>page2=879 ------>medlineContent= ------>unit=E0105 ------>insert_date=20071130 ------>iam=5 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c= ------>score=500 ------>journal_name=Biochim Biophys Acta ------>paper_name=Switch activation of PI-PLC downstream signals in activated macrophages with wortmannin. ------>confirm_date=20080321 ------>tch_id=094065 ------>pmid=17488650 ------>page1=869 ------>fullAbstract=Phosphatidylinositol (4,5)-bisphosphate (PtdIns(4,5)P(2)) has been known to serve as a substrate for phosphatidylinositol 3-kinase (PI(3)K) and phosphoinositide-specific phospholipase C (PI-PLC), which can produce PtdIns(3,4,5)P(3) and inositol 1,4,5-trisphosphate (Ins(1,4,5)P(3)) and diacylglycerol (DAG), respectively. In this study, we elucidated the role of PI-PLC during the LPS-activated mouse macrophages RAW264.7 treated with PI(3)K inhibitor wortmannin. First, wortmannin treatment enhanced Ins(1,4,5)P(3) production and iNOS expression in LPS-activated macrophages. Inhibition of PI(3)K by p85 siRNA also showed an enhancement of iNOS expression. On the other hand, overexpression of PI(3)K by ras-p110 expression plasmid significantly decreased iNOS expression in LPS-activated macrophages. In addition, overexpression of wild-type or dominant-negative Akt expression plasmid did not affect the iNOS expression in LPS-activated macrophages. Second, treatment of PI-PLC inhibitor U73122 reversed the enhancement of iNOS expression, the increase of phosphorylation level of ERK, JNK and p38, and the increase of AP-1-dependent gene expression in wortmannin-treated and LPS-activated macrophages. However, NF-kappaB activity determined by EMSA assay and reporter plasmid assay did not change during LPS-activated macrophages with or without wortmannin. We propose that the inhibition of PI(3)K by wortmannin in mouse macrophages enhances the PI-PLC downstream signals, and subsequently increases the LPS induction of iNOS expression independently of Akt pathway. ------>tmu_sno=None ------>sno=16311 ------>authors2=Liang HJ ------>authors3=Chen CH ------>authors4=Lin SY ------>authors5=Zhong WB ------>authors6=Ho FM, Hou WC, Lo JL, Ho YS, Lin PJ, Hung LF, Lian ------>authors6_c= ------>authors=Liu DZ ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Switch activation of PI-PLC downstream signals in activated macrophages with wortmannin. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no=6 ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2007 ------>submit_flag=None ------>publish_month=6 |