Claudia Colussi

@cnr.it

Department of engineering, Institute of System Analyis and Informatic
National Research Council- IASI

Claudia Colussi


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https://researchid.co/claudiacolussi

RESEARCH, TEACHING, or OTHER INTERESTS

Neuroscience, Cellular and Molecular Neuroscience, Developmental Neuroscience
60

Scopus Publications

Scopus Publications

  • Oxidative Stress and the Central Nervous System
    Marcello D’Ascenzo, Claudia Colussi
    Antioxidants, 2025
    Reactive oxygen and nitrogen species (ROS; RNS) are natural bioproducts of cellular metabolism, particularly produced within the mitochondria during energy production [...]
  • SUMOylation balance: a key determinant in synapse physiology
    Alessia Bertozzi, Walter Toscanelli, Giuditta Castellitto, Claudio Grassi, Claudia Colussi
    Frontiers in Physiology, 2025
    Neuronal communication relies on the precise regulation of synaptic compartments, where protein activity, localization, and turnover are tightly controlled. Among the mechanisms ensuring this regulation, post-translational modifications (PTMs) play a central role. SUMOylation, the covalent attachment of Small Ubiquitin-like Modifier (SUMO) proteins to target substrates, has emerged as a dynamic key PTM in the nervous system, modulating synaptic structure and function. Target SUMOylation occurs through an enzymatic cascade and requires the presence of a consensus sequence. Reversible addition of SUMO monomers or chains may contribute to distinct functional outcomes changing the conformation of the protein thus favoring/inhibiting molecular interaction among proteins or stabilizing the protein inhibiting degradation or influencing subcellular localization. All these SUMO dependent effects are crucial in the regulation of the tiny and highly specialized synaptic compartments to achieve spatiotemporal control for proper neurotransmission and synaptic plasticity in response to environmental stimuli. Dysregulation of this system has been implicated in various neurological disorders, including Alzheimer’s disease, where imbalances in SUMO1 versus SUMO2/3 levels contribute to synaptic dysfunction. As such, comprehension of SUMO related mechanisms may give important insights into both physiological regulation of synapses and potential therapeutic approaches for neurodegenerative diseases. Thus, in this review we will first introduce the enzymatic cascade of SUMOylation and its impact on protein function, then we will focus on its role within the synaptic compartment. Finally, we will discuss the therapeutic potential of modulating SUMOylation in Alzheimer’s disease as example of neurodegenerative disorders.
  • Glycine-induced activation of GPR158 increases the intrinsic excitability of medium spiny neurons in the nucleus accumbens
    Giuseppe Aceto, Luca Nardella, Simona Nanni, Valeria Pecci, Alessia Bertozzi, Sofia Nutarelli, Maria Teresa Viscomi, Claudia Colussi, Marcello D’Ascenzo, Claudio Grassi
    Cellular and Molecular Life Sciences, 2024
    It has been recently established that GPR158, a class C orphan G protein-coupled receptor, serves as a metabotropic glycine receptor. GPR158 is highly expressed in the nucleus accumbens (NAc), a major input structure of the basal ganglia that integrates information from cortical and subcortical structures to mediate goal-directed behaviors. However, whether glycine modulates neuronal activity in the NAc through GPR158 activation has not been investigated yet. Using whole-cell patch-clamp recordings, we found that glycine-dependent activation of GPR158 increased the firing rate of NAc medium spiny neurons (MSNs) while it failed to significantly affect the excitability of cholinergic interneurons (CIN). In MSNs GPR158 activation reduced the latency to fire, increased the action potential half-width, and reduced action potential afterhyperpolarization, effects that are all consistent with negative modulation of potassium M-currents, that in the central nervous system are mainly carried out by Kv7/KCNQ-channels. Indeed, we found that the GPR158-induced increase in MSN excitability was associated with decreased M-current amplitude, and selective pharmacological inhibition of the M-current mimicked and occluded the effects of GPR158 activation. In addition, when the protein kinase A (PKA) or extracellular signal-regulated kinase (ERK) signaling was pharmacologically blocked, modulation of MSN excitability by GPR158 activation was suppressed. Moreover, GPR158 activation increased the phosphorylation of ERK and Kv7.2 serine residues. Collectively, our findings suggest that GPR158/PKA/ERK signaling controls MSN excitability via Kv7.2 modulation. Glycine-dependent activation of GPR158 may significantly affect MSN firing in vivo, thus potentially mediating specific aspects of goal-induced behaviors.
  • Structural and functional alterations of neurons derived from sporadic Alzheimer’s disease hiPSCs are associated with downregulation of the LIMK1-cofilin axis
    Raimondo Sollazzo, Domenica Donatella Li Puma, Giuseppe Aceto, Fabiola Paciello, Claudia Colussi, Maria Gabriella Vita, Guido Maria Giuffrè, Francesco Pastore, Alessia Casamassa, Jessica Rosati, Agnese Novelli, Sabrina Maietta, Francesco Danilo Tiziano, Camillo Marra, Cristian Ripoli, Claudio Grassi
    Alzheimer S Research and Therapy, 2024
    BACKGROUND: Alzheimer's Disease (AD) is a neurodegenerative disorder characterized by the accumulation of pathological proteins and synaptic dysfunction. This study aims to investigate the molecular and functional differences between human induced pluripotent stem cells (hiPSCs) derived from patients with sporadic AD (sAD) and age-matched controls (healthy subjects, HS), focusing on their neuronal differentiation and synaptic properties in order to better understand the cellular and molecular mechanisms underlying AD pathology. METHODS: Skin fibroblasts from sAD patients (n = 5) and HS subjects (n = 5) were reprogrammed into hiPSCs using non-integrating Sendai virus vectors. Through karyotyping, we assessed pluripotency markers (OCT4, SOX2, TRA-1-60) and genomic integrity. Neuronal differentiation was evaluated by immunostaining for MAP2 and NEUN. Electrophysiological properties were measured using whole-cell patch-clamp, while protein expression of Aβ, phosphorylated tau, Synapsin-1, Synaptophysin, PSD95, and GluA1 was quantified by western blot. We then focused on PAK1-LIMK1-Cofilin signaling, which plays a key role in regulating synaptic structure and function, both of which are disrupted in neurodegenerative diseases such as AD. RESULTS: sAD and HS hiPSCs displayed similar stemness features and genomic stability. However, they differed in neuronal differentiation and function. sAD-derived neurons (sAD-hNs) displayed increased levels of AD-related proteins, including Aβ and phosphorylated tau. Electrophysiological analyses revealed that while both sAD- and HS-hNs generated action potentials, sAD-hNs exhibited decreased spontaneous synaptic activity. Significant reductions in the expression of synaptic proteins such as Synapsin-1, Synaptophysin, PSD95, and GluA1 were found in sAD-hNs, which are also characterized by reduced neurite length, indicating impaired differentiation. Notably, sAD-hNs demonstrated a marked reduction in LIMK1 phosphorylation, which could be the underlying cause for the changes in cytoskeletal dynamics that we found, leading to the morphological and functional modifications observed in sAD-hNs. To further investigate the involvement of the LIMK1 pathway in the morphological and functional changes observed in sAD neurons, we conducted perturbation experiments using the specific LIMK1 inhibitor, BMS-5. Neurons obtained from healthy subjects treated with the inhibitor showed similar morphological changes to those observed in sAD neurons, confirming that LIMK1 activity is crucial for maintaining normal neuronal structure. Furthermore, administration of the inhibitor to sAD neurons did not exacerbate the morphological alterations, suggesting that LIMK1 activity is already compromised in these cells. CONCLUSION: Our findings demonstrate that although sAD- and HS-hiPSCs are similar in their stemness and genomic stability, sAD-hNs exhibit distinct functional and structural anomalies mirroring AD pathology. These anomalies include synaptic dysfunction, altered cytoskeletal organization, and accumulation of AD-related proteins. Our study underscores the usefulness of hiPSCs in modeling AD and provides insights into the disease's molecular underpinnings, thus highlighting potential therapeutic targets.
  • Nucleoporin 153 deficiency in adult neural stem cells defines a pathological protein-network signature and defective neurogenesis in a mouse model of AD
    Claudia Colussi, Alessia Bertozzi, Lucia Leone, Marco Rinaudo, Raimondo Sollazzo, Federica Conte, Elena Paccosi, Luca Nardella, Giuseppe Aceto, Domenica Donatella Li Puma, Cristian Ripoli, Maria Gabriella Vita, Camillo Marra, Marcello D’Ascenzo, Claudio Grassi
    Stem Cell Research and Therapy, 2024
    Background Reduction of adult hippocampal neurogenesis is an early critical event in Alzheimer’s disease (AD), contributing to progressive memory loss and cognitive decline. Reduced levels of the nucleoporin 153 (Nup153), a key epigenetic regulator of NSC stemness, characterize the neural stem cells isolated from a mouse model of AD (3×Tg) (AD-NSCs) and determine their altered plasticity and gene expression. Methods Nup153-regulated mechanisms contributing to NSC function were investigated: (1) in cultured NSCs isolated from AD and wild type (WT) mice by proteomics; (2) in vivo by lentiviral-mediated delivery of Nup153 or GFP in the hippocampus of AD and control mice analyzing neurogenesis and cognitive function; (3) in human iPSC-derived brain organoids obtained from AD patients and control subjects as a model of neurodevelopment. Results Proteomic approach identified Nup153 interactors in WT- and AD-NSCs potentially implicated in neurogenesis regulation. Gene ontology (GO) analysis showed that Nup153-bound proteins in WT-NSCs were involved in RNA metabolism, nuclear import and epigenetic mechanisms. Nup153-bound proteins in AD-NSCs were involved in pathways of neurodegeneration, mitochondrial dysfunction, proteasomal processing and RNA degradation. Furthermore, recovery of Nup153 levels in AD-NSCs reduced the levels of oxidative stress markers and recovered proteasomal activity. Lentiviral-mediated delivery of Nup153 in the hippocampal niche of AD mice increased the proliferation of early progenitors, marked by BrdU/DCX and BrdU/PSANCAM positivity and, later, the integration of differentiating neurons in the cell granule layer (BrdU/NeuN+ cells) compared with GFP-injected AD mice. Consistently, Nup153-injected AD mice showed an improvement of cognitive performance in comparison to AD-GFP mice at 1 month after virus delivery assessed by Morris Water Maze. To validate the role of Nup153 in neurogenesis we took advantage of brain organoids derived from AD-iPSCs characterized by fewer neuroepithelial progenitor loops and reduced differentiation areas. The upregulation of Nup153 in AD organoids recovered the formation of neural-like tubes and differentiation. Conclusions Our data suggest that the positive effect of Nup153 on neurogenesis is based on a complex regulatory network orchestrated by Nup153 and that this protein is a valuable disease target.
  • Interleukin 1β triggers synaptic and memory deficits in Herpes simplex virus type-1-infected mice by downregulating the expression of synaptic plasticity-related genes via the epigenetic MeCP2/HDAC4 complex
    Domenica Donatella Li Puma, Claudia Colussi, Bruno Bandiera, Giulia Puliatti, Marco Rinaudo, Sara Cocco, Fabiola Paciello, Agnese Re, Cristian Ripoli, Giovanna De Chiara, Alessia Bertozzi, Anna Teresa Palamara, Roberto Piacentini, Claudio Grassi
    Cellular and Molecular Life Sciences, 2023
    Extensive research provides evidence that neuroinflammation underlies numerous brain disorders. However, the molecular mechanisms by which inflammatory mediators determine synaptic and cognitive dysfunction occurring in neurodegenerative diseases (e.g., Alzheimer’s disease) are far from being fully understood. Here we investigated the role of interleukin 1β (IL-1β), and the molecular cascade downstream the activation of its receptor, to the synaptic dysfunction occurring in the mouse model of multiple Herpes simplex virus type-1 (HSV-1) reactivations within the brain. These mice are characterized by neuroinflammation and memory deficits associated with a progressive accumulation of neurodegenerative hallmarks (e.g., amyloid-β protein and tau hyperphosphorylation). Here we show that mice undergone two HSV-1 reactivations in the brain exhibited increased levels of IL-1β along with significant alterations of: (1) cognitive performances; (2) hippocampal long-term potentiation; (3) expression synaptic-related genes and pre- and post-synaptic proteins; (4) dendritic spine density and morphology. These effects correlated with activation of the epigenetic repressor MeCP2 that, in association with HDAC4, affected the expression of synaptic plasticity-related genes. Specifically, in response to HSV-1 infection, HDAC4 accumulated in the nucleus and promoted MeCP2 SUMOylation that is a post-translational modification critically affecting the repressive activity of MeCP2. The blockade of IL-1 receptors by the specific antagonist Anakinra prevented the MeCP2 increase and the consequent downregulation of gene expression along with rescuing structural and functional indices of neurodegeneration. Collectively, our findings provide novel mechanistic evidence on the role played by HSV-1-activated IL-1β signaling pathways in synaptic deficits leading to cognitive impairment.
  • Cytoplasmic HDAC4 recovers synaptic function in the 3×Tg mouse model of Alzheimer's disease
    Claudia Colussi, Giuseppe Aceto, Cristian Ripoli, Alessia Bertozzi, Domenica Donatella Li Puma, Elena Paccosi, Marcello D'Ascenzo, Claudio Grassi
    Neuropathology and Applied Neurobiology, 2023
    Early dysfunction in Alzheimer's disease (AD) is characterised by alterations of synapse structure and function leading to dysmorphic neurites, decreased spine density, impaired synaptic plasticity and cognitive deficits. The class II member HDAC4, which recently emerged as a crucial factor in shaping synaptic plasticity and memory, was found to be altered in AD. We investigated how the modulation of HDAC4 may contribute to counteracting AD pathogenesis.
  • Near-infrared controlled release of mesenchymal stem cells secretome from bioprinted graphenebased microbeads for nerve regeneration
    Giordano Perini, Valentina Palmieri, Marcello D’Ascenzo, Claudia Colussi, Claudio Grassi, Ginevra Friggeri, Alberto Augello, Lishan Cui, Massimiliano Papi, Marco De Spirito
    International Journal of Bioprinting, 2023
     Nerve damage is a prevalent and debilitating condition with limited treatment options. Recent years have seen an increased incidence of neural damage due to factors such as aging populations and traumatic brain injuries. Addressing the urgent need for effective therapies, this study explores the controlled delivery of mesenchymal stem cells (MSCs) secretome, a complex mixture of bioactive factors, which is currently being investigated for its potential in nerve regeneration. The secretome offers significant advantages over stem cells themselves, as it can be more easily characterized and controlled, enabling precise regulation of therapeutic interventions. However, the challenge lies in delivering the secretome specifically to the target anatomical region. To overcome this limitation, we propose a novel approach utilizing near-infrared (NIR) radiation-responsive bioprinted alginate-graphene oxide (AGO) microbeads. Graphene oxide (GO) is a highly biocompatible material with unique properties, including NIR responsiveness, enabling controlled release of therapeutic agents upon NIR exposure. We hypothesized that AGO microbeads could encapsulate MSCs secretome and release it in a controlled manner using NIR radiation. To investigate our hypothesis, controlled damage was induced to hippocampal neurons, and MSCs secretome was encapsulated within AGO microbeads. Subsequently, NIR radiation was applied to trigger the release of the secretome. We compared the efficacy of MSCs secretome with that of astrocytes, which also possess nerve growth and proliferation-promoting capabilities. Our findings demonstrated that the controlled release of MSCs secretome from AGO microbeads through non-invasive NIR radiation significantly promoted the proliferation and regeneration of neurons following nerve injury. AGO microbeads offer multiple advantages over conventional delivery methods, including precise control over the timing, location, and dosage of therapeutic agents. Furthermore, the potential for reduced immunogenicity and tumorigenicity enhances the safety profile of the therapy. Consequently, this study presents a promising avenue for the development of MSC-based therapies for nerve regeneration, with implications for the treatment of various neuropathies and injuries.  
  • Acute restraint stress impairs histamine type 2 receptor ability to increase the excitability of medium spiny neurons in the nucleus accumbens
    Giuseppe Aceto, Luca Nardella, Giacomo Lazzarino, Barbara Tavazzi, Alessia Bertozzi, Simona Nanni, Claudia Colussi, Marcello D'Ascenzo, Claudio Grassi
    Neurobiology of Disease, 2022
    Histamine, a monoamine implicated in stress-related arousal states, is synthesized in neurons exclusively located in the hypothalamic tuberomammillary nucleus (TMN) from where they diffusely innervate striatal and mesolimbic networks including the nucleus accumbens (NAc), a vital node in the limbic loop. Since histamine-containing TMN neuron output increases during stress, we hypothesized that exposure of mice to acute restrain stress (ARS) recruits endogenous histamine type 2 receptor (H2R) signaling in the NAc, whose activation increases medium spiny neurons (MSNs) intrinsic excitability via downregulation of A-type K + currents. We employed an ARS paradigm in which mice were restrained for 120 min, followed by a 20-min recovery period, after which brain slices were prepared for ex vivo electrophysiology. Using whole-cell patch-clamp recordings, we found that pharmacological activation of H2R failed to affect MSN excitability and A-type K + currents in mice that underwent ARS. Interestingly, in mice treated with H2R-antagonist prior to ARS paradigm, H2R activation increased evoked firing and decreased A-type K + currents similarly to what observed in control mice. Furthermore, H2R-antagonist treatment ameliorated anxiety-like behavior in ARS mice. Together, our findings indicate that ARS paradigm recruits endogenous H2R signaling in MSNs and suggest the involvement of H2R signaling in stress-related motivational states. • The nucleus accumbens is innervated by histaminergic fibers originated in the tuberomamillary nucleus. • Acute restraint stress (ARS) increases histamine levels in the NAc leading to saturation of H2R signaling pathway. • H2R antagonist treatment restores the ability of H2R signaling to modulate MSN excitability in mice exposed to ARS. • H2R antagonist treatment ameliorates anxiety-like behavior in ARS mice.
  • Activation of histamine type 2 receptors enhances intrinsic excitability of medium spiny neurons in the nucleus accumbens
    Giuseppe Aceto, Luca Nardella, Simona Nanni, Valeria Pecci, Alessia Bertozzi, Claudia Colussi, Marcello D'Ascenzo, Claudio Grassi
    Journal of Physiology, 2022
    Histaminergic neurons are exclusively located in the hypothalamic tuberomammillary nucleus, from where they project to many brain areas including the nucleus accumbens (NAc), a brain area that integrates diverse monoaminergic inputs to coordinate motivated behaviours. While the NAc expresses various histamine receptor subtypes, the mechanisms by which histamine modulates NAc activity are still poorly understood. Using whole‐cell patch‐clamp recordings, we found that pharmacological activation of histamine 2 (H2) receptors elevates the excitability of NAc medium spiny neurons (MSNs), while activation of H1 receptors failed to significantly affect MSN excitability. The evoked firing of MSNs increased after seconds of local H2 agonist administration and remained elevated for minutes. H2 receptor (H2R) activation accelerated subthreshold depolarization in response to current injection, reduced the latency to fire, diminished action potential afterhyperpolarization and increased the action potential half‐width. The increased excitability was protein kinase A‐dependent and associated with decreased A‐type K+ currents. In addition, selective pharmacological inhibition of the Kv4.2 channel, the main molecular determinant of A‐type K+ currents in MSNs, mimicked and occluded the increased excitability induced by H2R activation. Our results indicate that histaminergic transmission in the NAc increases MSN intrinsic excitability through H2R‐dependent modulation of Kv4.2 channels. Activation of H2R will significantly alter spike firing in MSNs in vivo, and this effect could be an important mechanism by which these receptors mediate certain aspects of goal‐induced behaviours.
  • Epigenetic regulation of neural stem cells: The emerging role of nucleoporins
    Claudia Colussi, Claudio Grassi
    Stem Cells, 2021
  • Connexin hemichannel activation by s-nitrosoglutathione synergizes strongly with photodynamic therapy potentiating anti-tumor bystander killing
    Chiara Nardin, Chiara Peres, Sabrina Putti, Tiziana Orsini, Claudia Colussi, Flavia Mazzarda, Marcello Raspa, Ferdinando Scavizzi, Anna Maria Salvatore, Francesco Chiani, Abraham Tettey-Matey, Yuanyuan Kuang, Guang Yang, Mauricio A. Retamal, Fabio Mammano
    Cancers, 2021
  • Enhancing Plasticity Mechanisms in the Mouse Motor Cortex by Anodal Transcranial Direct-Current Stimulation: The Contribution of Nitric Oxide Signaling
    Saviana Antonella Barbati, Sara Cocco, Valentina Longo, Matteo Spinelli, Katia Gironi, Andrea Mattera, Fabiola Paciello, Claudia Colussi, Maria Vittoria Podda, Claudio Grassi
    Cerebral Cortex, 2020
  • Chronic mild stress alters synaptic plasticity in the nucleus accumbens through GSK3β-dependent modulation of Kv4.2 channels
    Giuseppe Aceto, Claudia Colussi, Lucia Leone, Salvatore Fusco, Marco Rinaudo, Federico Scala, Thomas A. Green, Fernanda Laezza, Marcello D’Ascenzo, Claudio Grassi
    Proceedings of the National Academy of Sciences of the United States of America, 2020
  • Erratum: GSK3β Modulates Timing-Dependent Long-Term Depression Through Direct Phosphorylation of Kv4.2 Channels (Cerebral Cortex (bhy042) DOI: 10.1093/cercor/bhy042)
    Giuseppe Aceto, Agnese Re, Andrea Mattera, Lucia Leone, Claudia Colussi, Marco Rinaudo, Federico Scala, Katia Gironi, Saviana Antonella Barbati, Salvatore Fusco, Thomas Green, Fernanda Laezza, Marcello D’Ascenzo, Claudio Grassi
    Cerebral Cortex, 2019
  • Altered Nup153 Expression Impairs the Function of Cultured Hippocampal Neural Stem Cells Isolated from a Mouse Model of Alzheimer’s Disease
    Lucia Leone, Claudia Colussi, Katia Gironi, Valentina Longo, Salvatore Fusco, Domenica Donatella Li Puma, Marcello D’Ascenzo, Claudio Grassi
    Molecular Neurobiology, 2019
  • GSK3β modulates timing-dependent long-term depression through direct phosphorylation of Kv4.2 channels
    Giuseppe Aceto, Agnese Re, Andrea Mattera, Lucia Leone, Claudia Colussi, Marco Rinaudo, Federico Scala, Katia Gironi, Saviana Antonella Barbati, Salvatore Fusco, Thomas Green, Fernanda Laezza, Marcello D’Ascenzo, Claudio Grassi
    Cerebral Cortex, 2019
  • Olfactory memory is enhanced in mice exposed to extremely low-frequency electromagnetic fields via Wnt/β-catenin dependent modulation of subventricular zone neurogenesis
    Alessia Mastrodonato, Saviana Antonella Barbati, Lucia Leone, Claudia Colussi, Katia Gironi, Marco Rinaudo, Roberto Piacentini, Christine A. Denny, Claudio Grassi
    Scientific Reports, 2018
  • Sildenafil normalizes MALAT1 level in diabetic cardiomyopathy
    Lorenza Bacci, Saviana A. Barbati, Claudia Colussi, Aurora Aiello, Andrea M. Isidori, Claudio Grassi, Alfredo Pontecorvi, Antonella Farsetti, Carlo Gaetano, Simona Nanni
    Endocrine, 2018
  • Nucleoporin 153 regulates estrogen-dependent nuclear translocation of endothelial nitric oxide synthase and estrogen receptor beta in prostate cancer
    Agnese Re, Claudia Colussi, Simona Nanni, Aurora Aiello, Lorenza Bacci, Claudio Grassi, Alfredo Pontecorvi, Antonella Farsetti
    Oncotarget, 2018
  • Olfactory receptors in semen and in the male tract: From proteome to proteins
    Domenico Milardi, Claudia Colussi, Giuseppe Grande, Federica Vincenzoni, Francesco Pierconti, Francesca Mancini, Silvia Baroni, Massimo Castagnola, Riccardo Marana, Alfredo Pontecorvi
    Frontiers in Endocrinology, 2018
  • Transcription factor CREM mediates high glucose response in cardiomyocytes and in a male mouse model of prolonged hyperglycemia
    Saviana A. Barbati, Claudia Colussi, Lorenza Bacci, Aurora Aiello, Agnese Re, Egidio Stigliano, Andrea M. Isidori, Claudio Grassi, Alfredo Pontecorvi, Antonella Farsetti, Carlo Gaetano, Simona Nanni
    Endocrinology, 2017
  • The nuclear pore protein Nup153 associates with chromatin and regulates cardiac gene expression in dystrophic mdx hearts
    Simona Nanni, Agnese Re, Cristian Ripoli, Aoife Gowran, Patrizia Nigro, Domenico D’Amario, Antonio Amodeo, Filippo Crea, Claudio Grassi, Alfredo Pontecorvi, Antonella Farsetti, Claudia Colussi
    Cardiovascular Research, 2016
  • Anacardic acid and thyroid hormone enhance cardiomyocytes production from undifferentiated mouse ES cells along functionally distinct pathways
    Agnese Re, Simona Nanni, Aurora Aiello, Serena Granata, Claudia Colussi, Giulia Campostrini, Francesco Spallotta, Stefania Mattiussi, Valentina Pantisano, Carmen D’Angelo, Annamaria Biroccio, Alessandra Rossini, Andrea Barbuti, Dario DiFrancesco, Francesco Trimarchi, Alfredo Pontecorvi, Carlo Gaetano, Antonella Farsetti
    Endocrine, 2016
  • Anodal transcranial direct current stimulation boosts synaptic plasticity and memory in mice via epigenetic regulation of Bdnf expression
    Maria Vittoria Podda, Sara Cocco, Alessia Mastrodonato, Salvatore Fusco, Lucia Leone, Saviana Antonella Barbati, Claudia Colussi, Cristian Ripoli, Claudio Grassi
    Scientific Reports, 2016
  • Acetylation mediates Cx43 reduction caused by electrical stimulation
    Viviana Meraviglia, Valerio Azzimato, Claudia Colussi, Maria Cristina Florio, Anna Binda, Alice Panariti, Khaled Qanud, Silvia Suffredini, Laura Gennaccaro, Michele Miragoli, Andrea Barbuti, Paul D. Lampe, Carlo Gaetano, Peter P. Pramstaller, Maurizio C. Capogrossi, Fabio A. Recchia, Giulio Pompilio, Ilaria Rivolta, Alessandra Rossini
    Journal of Molecular and Cellular Cardiology, 2015
  • Adventitial vessel growth and progenitor cells activation in an ex vivo culture system mimicking human saphenous vein wall strain after coronary artery bypass grafting
    Francesca Prandi, Marco Piola, Monica Soncini, Claudia Colussi, Yuri D’Alessandra, Eleonora Penza, Marco Agrifoglio, Maria Cristina Vinci, Gianluca Polvani, Carlo Gaetano, Gianfranco Beniamino Fiore, Maurizio Pesce
    Plos One, 2015
  • The histone acetylase activator pentadecylidenemalonate 1b rescues proliferation and differentiation in the human cardiac mesenchymal cells of type 2 diabetic patients
    Matteo Vecellio, Francesco Spallotta, Simona Nanni, Claudia Colussi, Chiara Cencioni, Anja Derlet, Beatrice Bassetti, Manuela Tilenni, Maria Cristina Carena, Antonella Farsetti, Gianluca Sbardella, Sabrina Castellano, Antonello Mai, Fabio Martelli, Giulio Pompilio, Maurizio C. Capogrossi, Alessandra Rossini, Stefanie Dimmeler, Andreas Zeiher, Carlo Gaetano
    Diabetes, 2014
  • Detrimental effect of class-selective histone deacetylase inhibitors during tissue regeneration following hindlimb ischemia
    Francesco Spallotta, Silvia Tardivo, Simona Nanni, Jessica D. Rosati, Stefania Straino, Antonello Mai, Matteo Vecellio, Sergio Valente, Maurizio C. Capogrossi, Antonella Farsetti, Julie Martone, Irene Bozzoni, Alfredo Pontecorvi, Carlo Gaetano, Claudia Colussi
    Journal of Biological Chemistry, 2013
  • Estrogen-Dependent Dynamic Profile of eNOS-DNA Associations in Prostate Cancer
    Simona Nanni, Aurora Aiello, Agnese Re, Alessandro Guffanti, Valentina Benvenuti, Claudia Colussi, Luis Jaime Castro-Vega, Armando Felsani, Arturo Londono-Vallejo, Maurizio C. Capogrossi, Silvia Bacchetti, Carlo Gaetano, Alfredo Pontecorvi, Antonella Farsetti
    Plos One, 2013
  • A nitric oxide-dependent cross-talk between class i and III histone deacetylases accelerates skin repair
    Francesco Spallotta, Chiara Cencioni, Stefania Straino, Simona Nanni, Jessica Rosati, Simona Artuso, Isabella Manni, Claudia Colussi, Giulia Piaggio, Fabio Martelli, Sergio Valente, Antonello Mai, Maurizio C. Capogrossi, Antonella Farsetti, Carlo Gaetano
    Journal of Biological Chemistry, 2013
  • P300/CBP associated factor regulates nitroglycerin-dependent arterial relaxation by nε-lysine acetylation of contractile proteins
    Claudia Colussi, Alessandro Scopece, Serena Vitale, Francesco Spallotta, Stefania Mattiussi, Jessica Rosati, Barbara Illi, Antonello Mai, Sabrina Castellano, Gianluca Sbardella, Antonella Farsetti, Maurizio C. Capogrossi, Carlo Gaetano
    Arteriosclerosis Thrombosis and Vascular Biology, 2012
  • Silencing of GSTP1, a prostate cancer prognostic gene, by the estrogen receptor-β and endothelial nitric oxide synthase complex
    A. Re, A. Aiello, S. Nanni, A. Grasselli, V. Benvenuti, V. Pantisano, L. Strigari, C. Colussi, S. Ciccone, A. P. Mazzetti, F. Pierconti, F. Pinto, P. Bassi, M. Gallucci, S. Sentinelli, F. Trimarchi, S. Bacchetti, A. Pontecorvi, M. Lo Bello, A. Farsetti
    Molecular Endocrinology, 2011
  • NO points to epigenetics in vascular development
    B. Illi, C. Colussi, J. Rosati, F. Spallotta, S. Nanni, A. Farsetti, M. C. Capogrossi, C. Gaetano
    Cardiovascular Research, 2011
  • Smad-interacting protein-1 and microRNA 200 family define a nitric oxide-dependent molecular circuitry involved in embryonic stem cell mesendoderm differentiation
    Jessica Rosati, Francesco Spallotta, Simona Nanni, Annalisa Grasselli, Annalisa Antonini, Sara Vincenti, Carlo Presutti, Claudia Colussi, Carmen D'Angelo, Anna Biroccio, Antonella Farsetti, Maurizio C. Capogrossi, Barbara Illi, Carlo Gaetano
    Arteriosclerosis Thrombosis and Vascular Biology, 2011
  • Nε-lysine acetylation determines dissociation from GAP junctions and lateralization of connexin 43 in normal and dystrophic heart
    Claudia Colussi, Jessica Rosati, Stefania Straino, Francesco Spallotta, Roberta Berni, Donatella Stilli, Stefano Rossi, Ezio Musso, Emilio Macchi, Antonello Mai, Gianluca Sbardella, Sabrina Castellano, Cristina Chimenti, Andrea Frustaci, Angela Nebbioso, Lucia Altucci, Maurizio C. Capogrossi, Carlo Gaetano
    Proceedings of the National Academy of Sciences of the United States of America, 2011
  • Histone deacetylase inhibitors: Keeping momentum for neuromuscular and cardiovascular diseases treatment
    Claudia Colussi, Barbara Illi, Jessica Rosati, Francesco Spallotta, Antonella Farsetti, Annalisa Grasselli, Antonello Mai, Maurizio C. Capogrossi, Carlo Gaetano
    Pharmacological Research, 2010
  • The histone deacetylase inhibitor suberoylanilide hydroxamic acid reduces cardiac arrhythmias in dystrophic mice
    Claudia Colussi, Roberta Berni, Jessica Rosati, Stefania Straino, Serena Vitale, Francesco Spallotta, Silvana Baruffi, Leonardo Bocchi, Francesca Delucchi, Stefano Rossi, Monia Savi, Dante Rotili, Federico Quaini, Emilio Macchi, Donatella Stilli, Ezio Musso, Antonello Mai, Carlo Gaetano, Maurizio C. Capogrossi
    Cardiovascular Research, 2010
  • Proteomic profile of differentially expressed plasma proteins from dystrophic mice and following suberoylanilide hydroxamic acid treatment
    C. Colussi, C. Banfi, M. Brioschi, E. Tremoli, S. Straino, F. Spallotta, Antonello Mai, Dante Rotili, M. C. Capogrossi, Carlo Gaetano
    Proteomics Clinical Applications, 2010
  • Common micro-RNA signature in skeletal muscle damage and regeneration induced by Duchenne muscular dystrophy and acute ischemia
    Simona Greco, Marco De Simone, Claudia Colussi, Germana Zaccagnini, Pasquale Fasanaro, Mario Pescatori, Rosanna Cardani, Riccardo Perbellini, Eleonora Isaia, Patrizio Sale, Giovanni Meola, Maurizio C. Capogrossi, Carlo Gaetano, Fabio Martelli
    FASEB Journal, 2009
  • NO sparks off chromatin: Tales of a multifaceted epigenetic regulator
    Barbara Illi, Claudia Colussi, Annalisa Grasselli, Antonella Farsetti, Maurizio C. Capogrossi, Carlo Gaetano
    Pharmacology and Therapeutics, 2009
  • Nitric oxide deficiency determines global chromatin changes in Duchenne muscular dystrophy
    Claudia Colussi, Aymone Gurtner, Jessica Rosati, Barbara Illi, Gianluca Ragone, Giulia Piaggio, Maurizio Moggio, Costanza Lamperti, Grazia D'Angelo, Emilio Clementi, Giulia Minetti, Chiara Mozzetta, Annalisa Antonini, Maurizio C. Capogrossi, Pier Lorenzo Puri, Carlo Gaetano
    FASEB Journal, 2009
  • Endothelial NOS, estrogen receptor β, and HIFs cooperate in the activation of a prognostic transcriptional pattern in aggressive human prostate cancer
    Simona Nanni, Valentina Benvenuti, Annalisa Grasselli, Carmen Priolo, Aurora Aiello, Stefania Mattiussi, Claudia Colussi, Vittoria Lirangi, Barbara Illi, Manuela D’Eletto, Anna Maria Cianciulli, Michele Gallucci, Piero De Carli, Steno Sentinelli, Marcella Mottolese, Paolo Carlini, Lidia Strigari, Stephen Finn, Elke Mueller, Giorgio Arcangeli, Carlo Gaetano, Maurizio C. Capogrossi, Raffaele Perrone Donnorso, Silvia Bacchetti, Ada Sacchi, Alfredo Pontecorvi, Massimo Loda, Antonella Farsetti
    Journal of Clinical Investigation, 2009
  • Erratum: HDAC2 blockade by nitric oxide and histone deacetylase inhibitors reveals a common target in Duchenne muscular dystrophy treatment (Proceedings of the National Academy of Sciences of the United States of America (2008) 105 (19183-19187) DOI: 10.1073/pnas.0805514105))
    Proceedings of the National Academy of Sciences of the United States of America, 2009
  • HDAC2 blockade by nitric oxide and histone deacetylase inhibitors reveals a common target in Duchenne muscular dystrophy treatment
    Claudia Colussi, Chiara Mozzetta, Aymone Gurtner, Barbara Illi, Jessica Rosati, Stefania Straino, Gianluca Ragone, Mario Pescatori, Germana Zaccagnini, Annalisa Antonini, Giulia Minetti, Fabio Martelli, Giulia Piaggio, Paola Gallinari, Christian Steinkuhler, Emilio Clementi, Carmela Dell'Aversana, Lucia Altucci, Antonello Mai, Maurizio C. Capogrossi, Pier Lorenzo Puri, Carlo Gaetano
    Proceedings of the National Academy of Sciences of the United States of America, 2008
  • AAV-dependent targeting of myostatin function: Follistatin strikes back at muscular dystrophy
    C Colussi, C Gaetano, M C Capogrossi
    Gene Therapy, 2008
  • Estrogen receptor-α and endothelial nitric oxide synthase nuclear complex regulates transcription of human telomerase
    Annalisa Grasselli, Simona Nanni, Claudia Colussi, Aurora Aiello, Valentina Benvenuti, Gianluca Ragone, Fabiola Moretti, Ada Sacchi, Silvia Bacchetti, Carlo Gaetano, Maurizio C. Capogrossi, Alfredo Pontecorvi, Antonella Farsetti
    Circulation Research, 2008
  • NF-Y dependent epigenetic modifications discriminate between proliferating and postmitotic tissue
    Aymone Gurtner, Paola Fuschi, Fiorenza Magi, Claudia Colussi, Carlo Gaetano, Matthias Dobbelstein, Ada Sacchi, Giulia Piaggio
    Plos One, 2008
  • Nitric oxide modulates chromatin folding in human endothelial cells via protein phosphatase 2A activation and class II histone deacetylases nuclear shuttling
    Barbara Illi, Claudio Dello Russo, Claudia Colussi, Jessica Rosati, Michele Pallaoro, Francesco Spallotta, Dante Rotili, Sergio Valente, Gianluca Ragone, Fabio Martelli, Paolo Biglioli, Christian Steinkuhler, Paola Gallinari, Antonello Mai, Maurizio C. Capogrossi, Carlo Gaetano
    Circulation Research, 2008
  • PEDF, PPAR-γ, p53: Deadly circuits arise when worlds collide
    C GAETANO, C COLUSSI, M CAPOGROSSI
    Cardiovascular Research, 2007
  • Functional and morphological recovery of dystrophic muscles in mice treated with deacetylase inhibitors
    G C Minetti, C Colussi, R Adami, C Serra, C Mozzetta, V Parente, S Fortuni, S Straino, M Sampaolesi, M Di Padova, B Illi, P Gallinari, C Steinkühler, M C Capogrossi, V Sartorelli, R Bottinelli, C Gaetano, P L Puri
    Nature Medicine, 2006
  • Senescence and death of primitive cells and myocytes lead to premature cardiac aging and heart failure
    Cristina Chimenti, Jan Kajstura, Daniele Torella, Konrad Urbanek, Hubert Heleniak, Claudia Colussi, Franca Di Meglio, Bernardo Nadal-Ginard, Andrea Frustaci, Annarosa Leri, Attilio Maseri, Piero Anversa
    Circulation Research, 2003
  • The Mammalian Mismatch Repair pathway removes DNA 8-oxodGMP incorporated from the oxidized dNTP pool
    Claudia Colussi, Eleonora Parlanti, Paolo Degan, Gabriele Aquilina, Deborah Barnes, Peter Macpherson, Peter Karran, Marco Crescenzi, Eugenia Dogliotti, Margherita Bignami
    Current Biology, 2002
  • 1,2-Dimethylhydrazine-induced colon carcinoma and lymphoma in msh2-/- mice
    C. Colussi, S. Fiumicino, A. Giuliani, S. Rosini, P. Musiani, C. Macri, C. S. Potten, M. Crescenzi, M. Bignami
    Journal of the National Cancer Institute, 2001
  • Hypersensitivity to camptothecin in MSH2 deficient cells is correlated with a role for MSH2 protein in recombinational repair
    Pietro Pichierri, Annapaola Franchitto, Rita Piergentili, Claudia Colussi, Fabrizio Palitti
    Carcinogenesis, 2001
  • Sensitivity to DNA cross-linking chemotherapeutic agents in mismatch repair-defective cells in vitro and in xenografts
    Silvia Fiumicino, Simone Martinelli, Claudia Colussi, Gabriele Aquilina, Carlo Leonetti, Marco Crescenzi, Margherita Bignami
    International Journal of Cancer, 2000
  • H2O2-induced block of glycolysis as an active ADP-ribosylation reaction protecting cells from apoptosis
    C. Colussi, M.C. Albertini, S. Coppola, S. Rovidati, F. Galli, L. Ghibelli
    FASEB Journal, 2000
  • Magnetic fields increase cell survival by inhibiting apoptosis via modulation of Ca2+ influx
    C. FANELLI, S. COPPOLA, R. BARONE, C. COLUSSI, G. GUALANDI, P. VOLPE, L. GHIBELLI
    FASEB Journal, 1999
  • Rescue of cells from apoptosis by inhibition of active GSH extrusion
    L. Ghibelli, C. Fanelli, G. Rotilio, E. Lafavia, S. Coppola, C. Colussi, P. Civitareale, M. R. Ciriolo
    FASEB Journal, 1998
  • ADP-Ribosylations in oxidative stress-induced apoptosis
    S. Coppola, C. Colussi, C. Albertini, S. Rovidati, F. Canestrari, L. Ghibelli
    Biochemical Society Transactions, 1996