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122 results on '"Ruberti F"'

5. MicroRNA Landscape in Alzheimer's Disease

Author

Cogoni C, Ruberti F, and Barbato C

Subjects
MicroRNAs, gene silencing, microRNA, Alzheimer Disease, Alzheimer, Brain, Humans, microRNA, Alzheimer, gene silencing
Abstract

Individual microRNAs and/or microRNA signatures were associated with AD. We report here the recent advances brought to the identification of microRNA changes in Alzheimer's disease (AD) brain and their biological function in the molecular pathways associated with the disease. This field represents a fertile route to understand the pathogenic mechanisms underlying Alzheimer's disease. In addition we review recent studies aimed to discover promising biomarkers for AD diagnosis by microRNA expression profiles of biofluids from AD patients.

Published
2015
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6. Selective inhibition of miR-92 in hippocampal neurons alters contextual fear memory

Author

Vetere, G., Barbato, C., Pezzola, S., Frisone, P., Aceti, M., Ciotti, M. T., Cogoni, Carlo, Ammassari Teule, M., and Ruberti, F.

Subjects
Neurons, Symporters, MEF2 Transcription Factors, Dendritic Spines, Conditioning, Classical, RNA-Binding Proteins, Fear, Hippocampus, Mice, Inbred C57BL, MicroRNAs, Memory, Animals, Rats, Wistar, Cells, Cultured
Abstract

Post-transcriptional gene regulation mediated by microRNAs (miRNAs) is implicated in memory formation; however, the function of miR-92 in this regulation is uncharacterized. The present study shows that training mice in contextual fear conditioning produces a transient increase in miR-92 levels in the hippocampus and decreases several miR-92 gene targets, including: (i) the neuronal Cl(-) extruding K(+) Cl(-) co-transporter 2 (KCC2) protein; (ii) the cytoplasmic polyadenylation protein (CPEB3), an RNA-binding protein regulator of protein synthesis in neurons; and (iii) the transcription factor myocyte enhancer factor 2D (MEF2D), one of the MEF2 genes which negatively regulates memory-induced structural plasticity. Selective inhibition of endogenous miR-92 in CA1 hippocampal neurons, by a sponge lentiviral vector expressing multiple sequences imperfectly complementary to mature miR-92 under the control of the neuronal specific synapsin promoter, leads to up-regulation of KCC2, CPEB3 and MEF2D, impairs contextual fear conditioning, and prevents a memory-induced increase in the spine density. Taken together, the results indicate that neuronal-expressed miR-92 is an endogenous fine regulator of contextual fear memory in mice.

Published
2014

18. The effects of anti-nerve growth factor monoclonal antibodies on developing basal forebrain neurons are transient and reversible

Author

MOLNAR M, TONGIORGI E, AVIGNONE E, GONFLONI S, RUBERTI F, DOMENICI L, CATTANEO, ANTONINO, Molnar, M, Tongiorgi, E, Avignone, E, Gonfloni, S, Ruberti, F, Domenici, L, and Cattaneo, Antonino

Subjects
Time Factors, Cell Transplantation, Intraventricular, Wistar, Cell Count, Chick Embryo, PC12 Cells, Hippocampus, Antibodies, Injections, Choline O-Acetyltransferase, Prosencephalon, Antibody Specificity, Proto-Oncogene Proteins, Receptors, Nerve Growth Factor, Monoclonal, Cholinesterases, Animals, Nerve Growth Factors, Ciliary Neurotrophic Factor, Cell Size, Cerebral Cortex, Neurons, Hybridomas, Age Factors, Receptor Protein-Tyrosine Kinases, Cell Differentiation, Immunohistochemistry, Rats, Settore BIO/18 - Genetica, nervous system, Cholinergic Fibers, Biological Assay, Rats, Wistar, COS Cells, Receptor, trkA, Injections, Intraventricular, Receptors, Nerve Growth Factor, Antibodies, Monoclonal, Receptor, Ciliary Neurotrophic Factor, trkA, Receptor
Abstract

In order to reassess the role of nerve growth factor (NGF) on rat basal forebrain cholinergic neurons (BFCNs) survival and/or phenotype maturation during the early postnatal life, we immunoneutralized NGF in vivo. Hybridoma cells producing the neutralizing anti-NGF monoclonal antibody alphaD11 were implanted in the lateral ventricle of the rat at different postnatal ages (P2, P8 and P15) and the effects on the number and the soma size of cholinacetyltransferase (ChAT) positive neurons were analysed 1, 2 or 3 weeks after the injection. A marked decrease in the number and in the soma size of BFCNs was observed implanting hybridoma cells at P2 and performing the analysis 1 week later. These effects are reversed 3 weeks after the implant of hybridoma cells at P2. At this time point, the levels of alphaD11 antibodies in the brain parenchyma are still in a vast molar excess over endogenous NGF. No effects on BFCNs were observed implanting alphaD11 cells at P15 while LGN neurons showed marked shrinkage. Our results demonstrate that the reduction in the number of ChAT-positive neurons during the first two postnatal weeks of anti-NGF treatment is not due to cell death. We conclude that NGF is not a survival factor for BFCNs, and that the influence of NGF on BFCNs cell maturation during the first 2 postnatal weeks is transient and reversible. Our results on tyrosine kinase (Trk) coexpression, suggest that NGF may cooperate with other factors in the cholinergic phenotype differentiation and maintenance after the second postnatal week.

Published
1998

34. Diabetic cardiomyopathy and erythrocyte Na-H antiport

Author

Matteucci, Elena, DI BELLO, Vitantonio, Talarico, L., Bertoni, C., Cecere, M., Ruberti, F., Di Muro, C., Uncini Manganelli, C., Piazza, F., Casini, M., Giusti, Costantino, and Giampietro, Ottavio

Published
1995

42. Erytrocyte Na/H exchange and preclinical abnormalities of left ventricular diastolic filling in the diabetic heart. 29th annual meting of the E.S.C.I. Cambridge 2and-5th April 1995

Author

Matteucci, E, DI BELLO, Vitantonio, Di Muro, C, Talarico, L, Ruberti, F, Cecere, M, Piazza, F, Giorgi, D, Giusti, Costantino, Erytrocyte Na/H exchange, Giampietro O., and Cambridge 2and 5th April 1995, preclinical abnormalities of left ventricular diastolic filling in the diabetic h. e. a. r. t. 29th annual meting of the E. S. C. I.

Published
1995

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