Cecilia Marini

Dr. Cecilia Marini

IRCCS Ospedale Policlinico San Martino, 16131 Genova, Italy

Research Focus & Metrics

Academic Career Length

36Years (1991-Present)

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

Representative Publications

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1 March 1991 in JACC
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Journal Article
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EPEugenio Picano
Eugenio Picano
FLFabio Lattanzi
Fabio Lattanzi
AOAndrés Orlandini
Andrés Orlandini
CMCecilia Marini
Cecilia Marini
ALAntonio L'ABbate
Antonio L'ABbate

6 March 2017 in Nature Materials
Verified
Journal Article
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JMJosé Fernando Maya-Vetencourt
José Fernando Maya-Vetencourt
DGDiego Ghezzi
Diego Ghezzi
MAMaria Rosa Antognazza
Maria Rosa Antognazza
ECElisabetta Colombo
Elisabetta Colombo
MMMaurizio Mete
Maurizio Mete
FBFabio Benfenati
Fabio Benfenati
The degeneration of photoreceptors in the retina is one of the major causes of adult blindness in humans. Unfortunately, no effective clinical treatments exist for the majority of retinal degenerative disorders. Here we report on the fabrication and functional validation of a fully organic prosthesis for long-term in vivo subretinal implantation in the eye of Royal College of Surgeons rats, a widely recognized model of retinitis pigmentosa. Electrophysiological and behavioural analyses reveal a prosthesis-dependent recovery of light sensitivity and visual acuity that persists up to 6–10 months after surgery. The rescue of the visual function is accompanied by an increase in the basal metabolic activity of the primary visual cortex, as demonstrated by positron emission tomography imaging. Our results highlight the possibility of developing a new generation of fully organic, highly biocompatible and functionally autonomous photovoltaic prostheses for subretinal implants to treat degenerative blindness.

29 September 2011 in Proceedings of the National Academy of Sciences
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Journal Article
Closed access
SCSabrina Chiesa
Sabrina Chiesa
Silvia MorbelliSilvia Morbelli
Silvia Morbelli
SMSara Morando
Sara Morando
MMMichela Massollo
Michela Massollo
CMCecilia Marini
Cecilia Marini
AUAntonio Uccelli
Antonio Uccelli
Dendritic cells (DC) are highly specialized antigen-presenting cells characterized by the ability to prime T-cell responses. Mesenchymal stem cells (MSC) are adult stromal progenitor cells displaying immunomodulatory activities including inhibition of DC maturation in vitro. However, the specific impact of MSC on DC functions, upon in vivo administration, has never been elucidated. Here we show that murine MSC impair Toll-like receptor-4 induced activation of DC resulting in the inhibition of cytokines secretion, down-regulation of molecules involved in the migration to the lymph nodes, antigen presentation to CD4+T cells, and cross-presentation to CD8+T cells. These effects are associated with the inhibition of phosphorylation of intracellular mitogen-activated protein kinases. Intravenous administration of MSC decreased the number of CCR7 and CD49dβ1 expressing CFSE-labeled DC in the draining lymph nodes and hindered local antigen priming of DO11.10 ovalbumin-specific CD4+T cells. Upon labeling of DC with technetium-99m hexamethylpropylene amine oxime to follow their in vivo biodistribution, we demonstrated that intravenous injection of MSC blocks, almost instantaneously, the migration of subcutaneously administered ovalbumin-pulsed DC to the draining lymph nodes. These findings indicate that MSC significantly affect DC ability to prime T cells in vivo because of their inability to home to the draining lymph nodes and further confirm MSC potentiality as therapy for immune-mediated diseases.

19 December 2012 in Cell Cycle
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Journal Article
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RWRoberto Würth
Roberto Würth
APAlessandra Pattarozzi
Alessandra Pattarozzi
MGMonica Gatti
Monica Gatti
ABAdirana Bajetto
Adirana Bajetto
ACAlessandro Corsaro
Alessandro Corsaro
TULLIO FLORIOTULLIO FLORIO
TULLIO FLORIO
Cancer stem cell theory postulates that a small population of tumor-initiating cells is responsible for the development, progression and recurrence of several malignancies, including glioblastoma. In this perspective, tumor-initiating cells represent the most relevant target to obtain effective cancer treatment. Metformin, a first-line drug for type II diabetes, was reported to possess anticancer properties affecting the survival of cancer stem cells in breast cancer models. We report that metformin treatment reduced the proliferation rate of tumor-initiating cell-enriched cultures isolated from four human glioblastomas. Metformin also impairs tumor-initiating cell spherogenesis, indicating a direct effect on self-renewal mechanisms. Interestingly, analyzing by FACS the antiproliferative effects of metformin on CD133-expressing subpopulation, a component of glioblastoma cancer stem cells, a higher reduction of proliferation was observed as compared with CD133-negative cells, suggesting a certain degree of...

18 March 2015 in Oncotarget
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Journal Article
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GBGiovanna Bianchi
Giovanna Bianchi
RMRoberto Martella
Roberto Martella
Silvia RaveraSilvia Ravera
Silvia Ravera
CMCecilia Marini
Cecilia Marini
SCSelene Capitanio
Selene Capitanio
VLValter Longo
Valter Longo
Tumor chemoresistance is associated with high aerobic glycolysis rates and reduced oxidative phosphorylation, a phenomenon called “Warburg effect” whose reversal could impair the ability of a wide range of cancer cells to survive in the presence or absence of chemotherapy. In previous studies, Short-term-starvation (STS) was shown to protect normal cells and organs but to sensitize different cancer cell types to chemotherapy but the mechanisms responsible for these effects are poorly understood. We tested the cytotoxicity of Oxaliplatin (OXP) combined with a 48hour STS on the progression of CT26 colorectal tumors. STS potentiated the effects of OXP on the suppression of colon carcinoma growth and glucose uptake in both in vitro and in vivo models. In CT26 cells, STS down-regulated aerobic glycolysis, and glutaminolysis, while increasing oxidative phosphorylation. The STS-dependent increase in both Complex I and Complex II-dependent O2 consumption was associated with increased oxidative stress and reduced ATP synthesis. Chemotherapy caused additional toxicity, which was associated with increased succinate/Complex II-dependent O2 consumption, elevated oxidative stress and apoptosis .

15 November 2013 in Cell Cycle
Verified
Journal Article
Open access
CMCecilia Marini
Cecilia Marini
BSBarbara Salani
Barbara Salani
MMMichela Massollo
Michela Massollo
AAAdriana Agnese Amaro
Adriana Agnese Amaro
AEAlessia Isabella Esposito
Alessia Isabella Esposito
Gianmario SambucetiGianmario Sambuceti
Gianmario Sambuceti
Emerging evidence suggests that metformin, a widely used anti-diabetic drug, may be useful in the prevention and treatment of different cancers. In the present study, we demonstrate that metformin ...