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Titolo:
UP-REGULATION OF UROKINASE-TYPE PLASMINOGEN-ACTIVATOR BY ENDOGENOUS AND EXOGENOUS HIV-1 TAT PROTEIN IN TUMOR-CELL LINES DERIVED FROM BK VIRUS TAT-TRANSGENIC MICE
Autore:
RUSNATI M; COLTRINI D; CAMPIONI D; TANGHETTI E; CORALLINI A; BARBANTIBRODANO G; GIULIANI R; GIBELLINI D; PRESTA M;
Indirizzi:
UNIV BRESCIA,DEPT BIOMED SCI & BIOTECHNOL,CHAIR GEN PATHOL & IMMUNOL,VIA VALSABBINA 19 I-25123 BRESCIA ITALY UNIV BRESCIA,DEPT BIOMED SCI & BIOTECHNOL,CHAIR GEN PATHOL & IMMUNOL I-25123 BRESCIA ITALY UNIV FERRARA,INST MICROBIOL I-44100 FERRARA ITALY UNIV FERRARA,INTERDEPT CTR BIOTECHNOL I-44100 FERRARA ITALY UNIV BOLOGNA,CHAIR MICROBIOL BOLOGNA ITALY
Titolo Testata:
AIDS
fascicolo: 6, volume: 11, anno: 1997,
pagine: 727 - 736
SICI:
0269-9370(1997)11:6<727:UOUPBE>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN-IMMUNODEFICIENCY-VIRUS; FIBROBLAST GROWTH-FACTOR; LONG TERMINAL REPEAT; FACTOR RECEPTOR; KAPOSIS-SARCOMA; STIMULATES GROWTH; ENDOTHELIAL-CELLS; GENE-EXPRESSION; BASIC DOMAIN; T-CELLS;
Keywords:
HIV-1 TAT; PLASMINOGEN ACTIVATORS; PROTEOLYSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
74
Recensione:
Indirizzi per estratti:
Citazione:
M. Rusnati et al., "UP-REGULATION OF UROKINASE-TYPE PLASMINOGEN-ACTIVATOR BY ENDOGENOUS AND EXOGENOUS HIV-1 TAT PROTEIN IN TUMOR-CELL LINES DERIVED FROM BK VIRUS TAT-TRANSGENIC MICE", AIDS, 11(6), 1997, pp. 727-736

Abstract

Objective: To demonstrate that Tat modulates the plasminogen-dependent proteolytic activity of tumour cell lines derived from BK virus (BKV)/tat-transgenic mice by affecting the production of plasminogen activators (PA) and the PA inhibitor (PAI)-1 and to demonstrate that this occurs through mechanism(s) that are distinct from those responsible for transactivating activity of extracellular Tat. Design and methods: To assess whether endogenous Tat is responsible for PA activity in T53 adenocarcinoma cells, cell cultures were transfected with antisense Tat cDNA and evaluated for cell-associated PA activity by a plasmin chromogenic assay. The assay was also used to evaluate PA activity in T53 cells and T111 leiomyosarcoma cells stimulated by extracellular Tat. The type(s) of PA produced were identified by sodium dodecyl sulphate-polyacrylamide gel electrophoresis zymography. The levels of PAI-1 wereevaluated by Western blotting. Tat transactivating activity was measured by a chloramphenicol acetyltransferase (CAT) enzyme-linked immunosorbent assay in HL3T1 cells containing integrated copies of an HIV-1 long terminal repeat (LTR)-CAT plasmid. Results: Transfection of T53 cells with antisense Tar cDNA results in the decrease of Tat production and PA activity. Exogenously added Tat increases PA levels in T53 and in T111 cells. PA activity was identified as urokinase-type PA (uPA). Tat also increases the production of PAI-1 in T111 but not in T53 cells. Chloroquine and heparin have different affects on the LTR-CAT-transactivating and the PA-inducing activities of Tat. The fusion protein glutathione-S-transferase-Tat and the mutant Tat-1e, lacking the secondTat exon, cause LTR-CAT transactivation without stimulating uPA upregulation. Conclusions: Tat affects the fibrinolytic activity of tumour cell lines derived from BKV/tat-transgenic mice by modulating the production of both uPA and PAI-1 via autocrine and paracrine mechanisms ofaction. The capacity of Tat to modulate the plasminogen-dependent proteolytic activity of these tumour cell lines may contribute to their metastatic potential. The uPA-inducing activity of Tat depends upon specific biological and structural features of the Tat protein that are distinct from those responsible for its LTR-CAT-transactivating activity, suggesting distinct mechanisms of induction for the two biological responses.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 07:39:50