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120 results on '"Lauro, Giuliana"'

1. Features and Functions of Human Microglia Cells

Author

Gremo, Fulvia, Sogos, Valeria, Ennas, Maria Grazia, Meloni, Alessandra, Persichini, Tiziana, Colasanti, Marco, Lauro, Giuliana Maria, Filogamo, Guido, editor, Vernadakis, Antonia, editor, Gremo, Fulvia, editor, Privat, Alain M., editor, and Timiras, Paola S., editor

Published
1997
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10. Recombinant Nef protein induces inflammatory response and upregulation of inducible nitric oxide synthase expression in the murine microglial cell line BV-2

Author

MANGINO, GIORGIO, PERCARIO, ZULEMA ANTONIA, LEONE, STEFANO, LAURO, Giuliana Maria, AFFABRIS, Elisabetta, FAMIGLIETTI MARYLINDA, FIORUCCI GIANNA, ROMEO GIOVANNA, GEYER MATTHIAS, Mangino, Giorgio, Famiglietti, Marylinda, Fiorucci, Gianna, Percario, ZULEMA ANTONIA, Leone, Stefano, Romeo, Giovanna, Geyer, Matthia, Lauro, Giuliana Maria, and Affabris, Elisabetta

Subjects
retrovirus, Virology, Microbiology
Abstract

8th National Congress of the Italian Society of Virology – Orvieto, September 21-23, 2008

Published
2008

11. Involvement of the intracellular ion channel CLIC1 in microglia-mediatedbeta-amyloid-induced neurotoxicity

Author

NOVARINO G., FABRIZI C., TONINI R., MALCHIODI ALBEDI F., DENTI M.A., SACCHETTI B., PARADISI S., FERRONI A., CURMI P.M., BREIT S.N., MAZZANTI M., LAURO, Giuliana Maria, Novarino, G., Fabrizi, C., Tonini, R., MALCHIODI ALBEDI, F., Denti, M. A., Lauro, Giuliana Maria, Sacchetti, B., Paradisi, S., Ferroni, A., Curmi, P. M., Breit, S. N., and Mazzanti, M.

Abstract

It is widely believed that the inflammatory events mediated by microglialactivation contribute to several neurodegenerative processes. Alzheimer'sdisease, for example, is characterized by an accumulation of beta-amyloidprotein (Abeta) in neuritic plaques that are infiltrated by reactive microgliaand astrocytes. Although Abeta and its fragment 25-35 exert a direct toxiceffect on neurons, they also activate microglia. Microglial activation isaccompanied by morphological changes, cell proliferation, and release of variouscytokines and growth factors. A number of scientific reports suggest that theincreased proliferation of microglial cells is dependent on ionic membranecurrents and in particular on chloride conductances. An unusual chloride ionchannel known to be associated with macrophage activation is the chlorideintracellular channel-1 (CLIC1). Here we show that Abeta stimulation of neonatalrat microglia specifically leads to the increase in CLIC1 protein and to thefunctional expression of CLIC1 chloride conductance, both barely detectable onthe plasma membrane of quiescent cells. CLIC1 protein expression in microgliaincreases after 24 hr of incubation with Abeta, simultaneously with theproduction of reactive nitrogen intermediates and of tumor necrosis factor-alpha(TNF-alpha). We demonstrate that reducing CLIC1 chloride conductance by aspecific blocker [IAA-94(R(+)-[(6,7-dichloro-2-cyclopentyl-2,3-dihydro-2-methyl-1-oxo-1H-inden-5yl)-oxy]acetic acid)] prevents neuronal apoptosis in neurons cocultured withAbeta-treated microglia. Furthermore, we show that small interfering RNAs usedto knock down CLIC1 expression prevent TNF-alpha release induced by Abetastimulation. These results provide a direct link between Abeta-inducedmicroglial activation and CLIC1 functional expression.

Published
2004

12. RECEPTOR MACHINERY INVOLVED IN MBP-INDUCED ASTROCYTE ACTIVATIONVII International Congress of Neuroimmunology (International Society of Neuroimmunology

Author

BUSINARO R., FUMAGALLI L., LEONE, STEFANO, LAURO, Giuliana Maria, R. Businaro, Businaro, R., Fumagalli, L., Leone, Stefano, and Lauro, Giuliana Maria

Abstract

Our data suggest that MBP interacts with astroglial cells, priming their activation, as proven by HLA class II modulation and HO-1 induction. MBP binding seems to be mediated by LRP,an endocytosis-mediating receptor. Such an interaction is followed by an increase of intracellular ROS content which, possibly, is counteracted by HO-1 induction. Many reports outlined the expression of HO-1 in multiple sclerosis and EAE, but its role in these diseases is still unclear (Chakrabarty et al. 2003), even if a growing body of evidence suggests that overexpression of HO-1 may protect tissues from immune-mediated injury either through prevention of oxidative damage or via a local immunomodulatory influence on infiltrating inflammatory cells (Kapturczak et al., 2004).

Published
2004

13. alpha-Bisabolol, a nontoxic natural compound, strongly induces apoptosis in glioma cells

Author

CAVALIERI E., MARIOTTO S., FABRIZI C., DE PRATI A.C., GOTTARDO R., BERRA L.V., CIAMPA A.R., SUZUKI H., LEONE, STEFANO, LAURO, Giuliana Maria, Cavalieri, E., Mariotto, S., Fabrizi, C., DE PRATI, A. C., Gottardo, R., Leone, Stefano, Berra, L. V., Lauro, Giuliana Maria, Ciampa, A. R., and Suzuki, H.

Abstract

In this study, alpha-bisabolol, a sesquiterpene alcohol present in natural essential oil, was found to have a strong time- and dose-dependent cytotoxic effect on human and rat glioma cells. After 24 h of treatment with 2.5-3.5 microM alpha-bisabolol, the viability of these cells was reduced by 50% with respect to untreated cells. Furthermore, the viability of normal rat glial cells was not affected by treatment with alpha-bisabolol at the same concentrations as above. Glioma cells treated with high concentration of alpha-bisabolol (10 microM) resulted in a 100% cell death. Judging from hypo-G1 accumulation, poly(ADP-ribose) polymerase cleavage, and DNA ladder formation, the cytotoxicity triggered by alpha-bisabolol resulted from apoptosis induction. Moreover, the dissipation of mitochondrial-inner transmembrane potential and the release of cytochrome c from mitochondria indicated that, in these glioma cells, apoptosis occurred through an intrinsic pathway. As pointed out by the experimental results, alpha-bisabolol may be considered a novel compound able to inhibit glioma cell growth and survival.

Published
2004

42. Induction of Nitric Oxide Synthase mRNA Expression

Author

Colasanti, Marco, primary, Persichini, Tiziana, additional, Menegazzi, Marta, additional, Mariotto, Sofia, additional, Giordano, Emanuele, additional, Caldarera, Claudio M., additional, Sogos, Valeria, additional, Lauro, Giuliana M., additional, and Suzuki, Hisanori, additional

Published
1995
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48. Involvement of the Intracellular Ion Channel CLIC1 in Microglia-Mediated β-Amyloid-Induced Neurotoxicity.

Author

Novarino, Gaia, Fabrizi, Cinzia, Tonini, Raffaella, Denti, Michela A., Malchiodi-Albedi, Fiorella, Lauro, Giuliana M., Sacchetti, Benedetto, Paradisi, Silvia, Ferroni, Arnaldo, Curmi, Paul M., Breit, Samuel N., and Mazzanti, Michele

Subjects
CHLORIDE channels, AMYLOID beta-protein, ALZHEIMER'S disease, NEUROTOXICOLOGY, MICROGLIA
Abstract

It is widely believed that the inflammatory events mediated by microglial activation contribute to several neurodegenerative processes. Alzheimer's disease, for example, is characterized by an accumulation of β-amyloid protein (Aβ) in neuritic plaques that are infiltrated by reactive microglia and astrocytes. Although Aβ and its fragment 25-35 exert a direct toxic effect on neurons, they also activate microglia. Microglial activation is accompanied by morphological changes, cell proliferation, and release of various cytokines and growth factors. A number of scientific reports suggest that the increased proliferation of microglial cells is dependent on ionic membrane currents and in particular on chloride conductances. An unusual chloride ion channel known to be associated with macrophage activation is the chloride intracellular channel-1 (CLIC1). Here we show that Aβ stimulation of neonatal rat microglia specifically leads to the increase in CLIC1 protein and to the functional expression of CLIC1 chloride conductance, both barely detectable on the plasma membrane of quiescent cells. CLIC1 protein expression in microglia increases after 24 hr of incubation with Aβ, simultaneously with the production of reactive nitrogen intermediates and of tumor necrosis factor-a (TNF-α). We demonstrate that reducing CLIC1 chloride conductance by a specific blocker [IAA-94 (R(+)-[(6,7-dichloro-2-cyclopentyl-2,3-dihydro-2-methyl-l-oxo-1H-inden-5yl)-oxy] acetic acid)] prevents neuronal apoptosis in neurons cocultured with Aβ-treated microglia. Furthermore, we show that small interfering RNAs used to knock down CLIC1 expression prevent TNF-α release induced by Aβ stimulation. These results provide a direct link between Aβ-induced microglial activation and CLIC1 functional expression. [ABSTRACT FROM AUTHOR]

Published
2004
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