Monica Pibiri

Dr. Monica Pibiri

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Academic Career Length

30Years (1997-Present)

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

Representative Publications

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23 April 2008 in The FASEB Journal
Verified
Journal Article
Closed access
PDF file
APAndrea Perra
Andrea Perra
GSGabriella Simbula
Gabriella Simbula
MSMichela Simbula
Michela Simbula
MPMonica Pibiri
Monica Pibiri
MKMarta A. Kowalik
Marta A. Kowalik
Amedeo ColumbanoAmedeo Columbano
Amedeo Columbano
21 November 2006 in Apoptosis
Verified
Journal Article
Closed access
PDF file
GSGabriella Simbula
Gabriella Simbula
Amedeo ColumbanoAmedeo Columbano
Amedeo Columbano
GLG. M. Ledda-Columbano
G. M. Ledda-Columbano
LSL. Sanna
L. Sanna
MDM. Deidda
M. Deidda
MPMonica Pibiri
Monica Pibiri
1 April 2001 in The FASEB Journal
Verified
Journal Article
Closed access
MPMonica Pibiri
Monica Pibiri
GLGiovanna M. Ledda-Columbano
Giovanna M. Ledda-Columbano
CCCostanza Cossu
Costanza Cossu
GSGabriella Simbula
Gabriella Simbula
MMMarta Menegazzi
Marta Menegazzi
Amedeo ColumbanoAmedeo Columbano
Amedeo Columbano
25 October 2005 in Hepatology
Verified
Journal Article
Open access
PDF file
Amedeo ColumbanoAmedeo Columbano
Amedeo Columbano
GLGiovanna M. Ledda-Columbano
Giovanna M. Ledda-Columbano
MPMonica Pibiri
Monica Pibiri
CCCostanza Cossu
Costanza Cossu
Marta MenegazziMarta Menegazzi
Marta Menegazzi
JLJoseph Locker
Joseph Locker
: We previously observed that Gadd45β/MyD118, a member of the Gadd45 family of inducible factors, showed the strongest immediate-early induction common to two distinctive proliferation responses of the liver: (1) regeneration induced by surgical partial hepatectomy and (2) hyperplasia induced by the primary mitogen TCPOBOP, a ligand of the constitutive androstane receptor (CAR). Gadd45β is known to be stimulated by nuclear factor (NF) κB, which is activated by tumor necrosis factor alpha (TNFα) in the early response to partial hepatectomy. We therefore investigated whether TNFα and NFκB also stimulated Gadd45β as part of the response to CAR ligands, or whether activation occurred by an alternative pathway. TCPOBOP effects were characterized in three mouse genotypes: wild-type, TNFR1−/−, and TNFR1−/−TNFR2−/−. The results showed that TCPOBOP did not activate NFκB in any of the mice, but a strong induction of Gadd45β messenger RNA was observed in all three genotypes, where TCPOBOP also induced CyP2b10, a classical target gene of activated CAR, and cyclin D1, a proliferation linked gene. Thus, the absence of TNFR signaling and induction of NFκB did not impair CAR-mediated gene induction. Moreover, hepatocyte proliferation was strongly induced, and at significantly higher levels than wild type, in both TNFR1−/− and TNFR1−/−TNFR2−/− mice. Further studies evaluated TCPOBOP-induced gene expression in CAR−/− mice, by microarray expression profiling and Northern blot. The induced changes in gene expression, including the stimulation of Gadd45β, were almost completely abolished—hence all were mediated via CAR activation. In conclusion , in the liver, Gadd45β can be induced by a distinctive pathway that requires CAR and is independent of TNFα-NFκB. The greater induction of proliferation in TNFR-null mice suggests negative cross-talk between the CAR and TNFα-NFκB controls that regulate proliferation. (Hepatology 2005.)
1 January 2000 in The American Journal of Pathology
Verified
Journal Article
Closed access
GLGiovanna M. Ledda-Columbano
Giovanna M. Ledda-Columbano
MPMonica Pibiri
Monica Pibiri
RLRoberto Loi
Roberto Loi
APAndrea Perra
Andrea Perra
HSHisashi Shinozuka
Hisashi Shinozuka
Amedeo ColumbanoAmedeo Columbano
Amedeo Columbano
9 March 2011 in Hepatology
Verified
Journal Article
Open access
PDF file
MKMarta A. Kowalik
Marta A. Kowalik
CSChristian Saliba
Christian Saliba
MPMonica Pibiri
Monica Pibiri
APAndrea Perra
Andrea Perra
GLGiovanna M. Ledda-Columbano
Giovanna M. Ledda-Columbano
Amedeo ColumbanoAmedeo Columbano
Amedeo Columbano
The Hippo kinase cascade, a growth-suppressive pathway that ultimately antagonizes the transcriptional coactivator Yes-associated protein (YAP), has been shown in transgenic animals to orchestrate organ size regulation. The purpose of this study was to determine whether in non–genetically modified mice (1) the Hippo pathway is involved in the regulation of adaptive liver enlargement caused by the mitogen 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP), an agonist of constitutive androstane receptor and (2) a dysregulation of this pathway occurs during the development of chemically induced hepatocellular carcinoma (HCC). We show that liver enlargement caused by TCPOBOP was associated with an increase of YAP protein levels that paralleled the increase in 2-bromodeoxyuridine incorporation. Interestingly, when a second dose of TCPOBOP was given to mice with enlarged livers, no further increases in liver mass or YAP protein levels were observed, suggesting that the Hippo pathway prevents further growth of the hyperplastic liver. Viral-mediated exogenous expression of active YAP in mouse livers was able to partially overcome the block of hepatocyte proliferation. We also show that HCCs developed in mice given diethylnitrosamine and then subjected to repeated treatments with TCPOBOP had increased levels of YAP that were associated with down-regulation of microRNA 375, which is known to control YAP expression, and with enhanced levels of alpha-fetoprotein and connective tissue growth factor, two target genes of YAP. Conclusion: These results suggest that the Hippo pathway regulates adaptive liver enlargement and is probably inactivated in initiated cells that escape the suppressive constrain exerted on the surrounding normal tissue, thus allowing clonal expansion to HCC (HEPATOLOGY 2011;)