19 research outputs found
HIV-associated nephropathy, that is to say how HIV can play a direct role in the disorders of an organ system
Gli effetti di Tat sui podociti (iperplasia, attivazione del citoscheletro, redistribuzione della nefrina) costituiscono meccanismi potenziali del danno renale nei pazienti HIV-positivi
Tat reduces insulin-like growth factors binding proteins while increasing proliferation of human pocytes cultured in vitro
Infezione da coxsackievirus B e patologie autoimmuni: possibile ruolo della replicazione persistente di questi agenti virali in cellule endoteliali microvascolari
Infezione di cellule intestinali polarizzate da parte di coxsackievirus B: rilascio vettoriale della progenie virale attraverso la membrana apicale
Antibody response to fibronectin-binding adhesin FnbpA in patients with Staphylococcal aureus infections
We have analyzed antibody reactivity to a fibronectin-binding microbial surface component that recognizes
adhesive matrix molecules (MSCRAMM) in blood plasma collected from patients with staphylococcal infections.
All patients had elevated levels of anti-MSCRAMM antibodies compared to those of young children who,
presumably, had not been exposed to staphylococcal infections. The anti-MSCRAMM antibodies preferentially
reacted with the ligand-binding repeat domain of the adhesin. However, these antibodies did not inhibit fibronectin
binding. Essentially, all patients had antibodies which specifically recognized the fibronectin-MSCRAMM
complex but not the isolated components. Epitopes recognized by these anti-ligand-induced binding sites antibodies
were found in each repeat unit of the MSCRAMM. These results demonstrate that staphylococci have
bound fibronectin some time during infection and that each repeat unit in the MSCRAMM can engage in
ligand binding. Furthermore, our previously proposed model, suggesting that an unordered structure in the
MSCRAMM undergoes a conformational change upon ligand binding (K. House-Pompeo, Y. Xu, D. Joh, P. Speziale,
and M. Ho¨o¨k, J. Biol. Chem. 271:1379–1384, 1996), is presumably operational in patients during infections
Heparin-binding domain of human fibronectin binds HIV-1 gp120/160 and reduces virus infectivity
The synthesis of platelet-activating factor modulates chemotaxis of monocytes induced by HIV-1 Tat
Human podocytes express IGFBPs in vitro: their involvement in apoptotic effect of HIV-1 transactivator of transcription
Potentiation of the malignant phenotype of the undifferentiated ARO thyroid cell line by insertion of the bcl-2 gene
We have reported that bcl-2 is expressed in normal human thyroid epithelium and that its expression is down-regulated in undifferentiated thyroid tumors, Production of IL-6 was concomitantly down-regulated in these forms. Based on these observations, we analyzed whether insertion of bcl-2 would reverse the highly malignant phenotype of a thyroid cell line (ARO) derived from an undifferentiated carcinoma. This cell line fails to produce Bcl-2 and IL-6, By infection with a bcl-2 retroviral vector, ARO cells expressing bcl-2 (ARObcl-2) were obtained, Compared with parental cells, expression of bcl-2 was associated with enhancement of growth potential (DNA synthesis, in vitro proliferation rate, anchorage-independent growth in semi-solid media). Chemotaxis and invasive potential in Boyden chambers were also increased, bcl-2-expressing cells showed a reduced response to apoptotic stimuli (low-serum conditions or anti-neoplastic drugs), Large branched colonies were formed in Matrigel from ARObcl-2 cells but not from parental cells. Finally, ARObcl-2 cells showed a decreased latency of tumor appearance when injected into immunodeficient mice. Potentiation of the malignant phenotype of ARO cells by bcl-2 was not ascribed to altered expression of (i) cytokine/growth factors (IL-4, IL-6, IL-8, IL-10, IL-12, TGF-alpha, TGF-beta), (ii) thyroid specific transcripts (TG, TPO, TSH-R, PIGF, PAX-8) or (iii) genes influencing tumor aggressiveness [VEGF, HMGI (Y), HMGI-C], Our data indicate that bcl-2 potentiates the malignant phenotype of ARO cells not only by limiting the response to apoptotic stimuli but also by enhancing proliferation and tumor aggressiveness