| Ohe H, Takashiba S, Naruishi K, Chou HH, Hamada H, Nishimura F, Arai H, Murayama Y. |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=2.593 ------>paper_class3=2 ------>paper_class2=1 ------>vol=20 ------>confirm_bywho=seanlee ------>insert_bywho=hhchou ------>Jurnal_Rank=44.8 ------>authors4_c=None ------>comm_author= ------>patent_EDate=None ------>authors5_c=None ------>publish_day=1 ------>paper_class2Letter=None ------>page2=1082 ------>medlineContent= ------>unit=F0100 ------>insert_date=20010424 ------>iam=4 ------>update_date= ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c=None ------>score=500 ------>journal_name=Journal of Interferon Cytokine Research ------>paper_name=Tumor necrosis factor-alpha (TNF-alpha)-induced and interleukin-1 beta (IL-1 beta)-induced shedding of TNF receptors from gingival fibroblasts. ------>confirm_date=20060215 ------>tch_id=086008 ------>pmid=11152574 ------>page1=1077 ------>fullAbstract=Tumor necrosis factor-alpha (TNF-alpha) exerts its functions by binding two different receptors (TNFR55 and TNFR75). Both TNFR55 and TNFR75 exist in cell-associated and soluble forms. Soluble TNF receptors (sTNFR), sTNFR55 and sTNFR75, are proteolytically shed upon inflammatory stimuli and then modulate various TNF-alpha bioactivities. As human gingival fibroblasts (HGF) can be potential targets for TNF-alpha in inflamed gingiva, we hypothesized that HGF partially modulate the cellular responses to TNF-alpha by regulating their own TNFR. In this study, the kinetics of expression of cell-associated and soluble forms of both receptors from cultured HGF in response to proinflammatory cytokines TNF-alpha and interleukin-1 beta (IL-1 beta) were investigated in vitro. Both TNF-alpha and IL-1 beta upregulated the gene expression of TNFR75 and did not affect that of TNFR55. TNF-alpha and IL-1 beta decreased binding of [(125)I]TNF-alpha to HGF. Moreover, TNF-alpha and IL-1 beta upregulated the release of sTNFR75 from HGF but not that of sTNFR55. These results suggest that HGF under inflammatory conditions may contribute to the inactivation of circulating TNF-alpha through the preferential induction and shedding of TNFR75. ------>tmu_sno=None ------>sno=3625 ------>authors2= ------>authors3= ------>authors4= ------>authors5= ------>authors6= ------>authors6_c=None ------>authors=Ohe H, Takashiba S, Naruishi K, Chou HH, Hamada H, Nishimura F, Arai H, Murayama Y. ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=0 ------>updateTitle=Tumor necrosis factor-alpha (TNF-alpha)-induced and interleukin-1 beta (IL-1 beta)-induced shedding of TNF receptors from gingival fibroblasts. ------>language=2 ------>check_flag= ------>submit_date= ------>country=None ------>no=12 ------>patent_SDate=None ------>update_bywho= ------>publish_year=2000 ------>submit_flag= ------>publish_month=1 |