Lina  Ghibelli

Prof. Dr. Lina Ghibelli

Dipartimento di Biologia, Università di Roma Tor Vergata, Roma, Italy

Research Focus & Metrics

Academic Career Length

28Years (1999-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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2 March 2011 in Nanoscale
Verified
Journal Article
Closed access
PDF file
ICIvana Celardo
Ivana Celardo
JPJens Z. Pedersen
Jens Z. Pedersen
ETEnrico Traversa
Enrico Traversa
LGLina Ghibelli
Lina Ghibelli
Nanotechnology promises a revolution in pharmacology to improve or create ex novo therapies. Cerium oxide nanoparticles (nanoceria), well-known as catalysts, possess an astonishing pharmacological potential due to their antioxidant properties, deriving from a fraction of Ce3+ ions present in CeO2. These defects, compensated by oxygen vacancies, are enriched at the surface and therefore in nanosized particles. Reactions involving redox cycles between the Ce3+ and Ce4+ oxidation states allow nanoceria to react catalytically with superoxide and hydrogen peroxide, mimicking the behavior of two key antioxidant enzymes, superoxide dismutase and catalase, potentially abating all noxious intracellular reactive oxygen species (ROS) via a self-regenerating mechanism. Hence nanoceria, apparently well tolerated by the organism, might fight chronic inflammation and the pathologies associated with oxidative stress, which include cancer and neurodegeneration. Here we review the biological effects of nanoceria as they emerge from in vitro and in vivo studies, considering biocompatibility and the peculiar antioxidant mechanisms.

20 August 2015 in Nanoscale
Verified
Journal Article
Closed access
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FCFanny Caputo
Fanny Caputo
MNMilena De Nicola
Milena De Nicola
ASAndrzej Sienkiewicz
Andrzej Sienkiewicz
AGAnna Giovanetti
Anna Giovanetti
IBIgnacio Bejarano
Ignacio Bejarano
LGLina Ghibelli
Lina Ghibelli
CeO 2 nanoparticles may provide trouble-free sun protection.

15 March 2010 in International Journal of Cell Biology
Verified
Journal Article
Open access
PDF file
CCClaudia Cerella
Claudia Cerella
MDMarc Diederich
Marc Diederich
LGLina Ghibelli
Lina Ghibelli
Is an important second messenger participating in many cellular activities; when physicochemical insults deregulate its delicate homeostasis, it acts as an intrinsic stressor, producing/increasing cell damage. Damage elicits both repair and death responses; intriguingly, in those responses also participates as second messenger. This delineates a dual role for in cell stress, making difficult to separate the different and multiple mechanisms required for -mediated control of cell survival and apoptosis. Here we attempt to disentangle the two scenarios, examining on the one side, the events implicated in deregulated toxicity and the mechanisms through which this elicits reparative or death pathways; on the other, reviewing the role of as a messenger in the transduction of these same signaling events.

1 November 2000 in The FASEB Journal
Verified
Journal Article
Open access
PDF file
CCClaudia. Colussi
Claudia. Colussi
Maria Cristina AlbertiniMaria Cristina Albertini
Maria Cristina Albertini
SCSimona Coppola
Simona Coppola
SRS. Rovidati
S. Rovidati
FGFrancesco Galli
Francesco Galli
LGLina Ghibelli
Lina Ghibelli
H 2 O 2 treatment on U937 cells leads to the block of glycolytic flux and the inactivation of glyceraldehyde‐3‐phosphate‐dehydrogenase by a posttranslational modification (possibly ADP‐ribosylation). Glycolysis spontaneously reactivates after 2 h of recovery from oxidative stress; thereafter cells begin to undergo apoptosis. The specific ADP‐ribosylation inhibitor 3‐aminobenzamide inhibits the stress‐induced inactivation of glyceraldehyde‐3‐phosphate‐dehydrogenase and the block of glycolysis; concomitantly, it anticipates and increases apoptosis. Exogenous block of glycolysis (i.e., by culture in glucose‐free medium or with glucose analogs or after NAD depletion), turns the transient block into a stable one: this results in protection from apoptosis, even when downstream cell metabolism is kept active by the addition of pyruvate. All this evidence indicates that the stress‐induced block of glycolysis is not the result of a passive oxidative damage, but rather an active cell reaction programmed via ADP‐ribosylation for cell self‐defense.—Colussi, C., Albertini, M. C., Coppola, S., Rovidati, S., Galli, F., Ghibelli, L. H 2 O 2 ‐induced block of glycolysis as an active ADP‐ribosylation reaction protecting cells from apoptosis. FASEB J . 14, 2266‐2276 (2000)

1 November 1999 in The FASEB Journal
Verified
Journal Article
Closed access
LGLina Ghibelli
Lina Ghibelli
SCSimona Coppola
Simona Coppola
CFC. Fanelli
C. Fanelli
GRG. Rotilio
G. Rotilio
PCP. Civitareale
P. Civitareale
MCM. R. Ciriolo
M. R. Ciriolo

21 November 2007 in Journal of Pineal Research
Verified
Journal Article
Closed access
PDF file
FRFlavia Radogna
Flavia Radogna
SCSilvia Cristofanon
Silvia Cristofanon
LPLaura Paternoster
Laura Paternoster
MDMaria D’aLessio
Maria D’aLessio
MNMilena De Nicola
Milena De Nicola
LGLina Ghibelli
Lina Ghibelli