Daniele Catalucci

@article{pmid33488405,

title = {Peptide-Based Ŧargeting of the L-Ŧype Calcium Channel Corrects the Loss-of-Function Phenotype of Ŧwo Novel Mutations of the CACNA1 Gene Associated With Brugada Syndrome},

author = {V Di Mauro and P Ceriotti and F Lodola and N Salvarani and J Modica and M L Bang and A Mazzanti and C Napolitano and S G Priori and D Catalucci},

year  = {2020},

date = {2020-01-01},

journal = {Front Physiol},

volume = {11},

pages = {616819},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid31680489,

title = {Đisease modeling of a mutation in α-actinin 2 guides clinical therapy in hypertrophic cardiomyopathy},

author = {M Prondzynski and M D Lemoine and A T Zech and A Horváth and V Di Mauro and J T Koivumäki and N Kresin and J Busch and T Krause and E Krämer and S Schlossarek and M Spohn and F W Friedrich and J Münch and S D Laufer and C Redwood and A E Volk and A Hansen and G Mearini and D Catalucci and C Meyer and T Christ and M Patten and T Eschenhagen and L Carrier},

year  = {2019},

date = {2019-01-01},

journal = {EMBO Mol Med},

volume = {11},

number = {12},

pages = {e11115},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid31249372,

title = {Wnt signalling mediates miR-133a nuclear re-localization for the transcriptional control of Đnmt3b in cardiac cells},

author = {V Di Mauro and S Crasto and F S Colombo and E Di Pasquale and D Catalucci},

year  = {2019},

date = {2019-01-01},

journal = {Sci Rep},

volume = {9},

number = {1},

pages = {9320},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid29343624,

title = {Inhalation of peptide-loaded nanoparticles improves heart failure},

author = {M Miragoli and P Ceriotti and M Iafisco and M Vacchiano and N Salvarani and A Alogna and P Carullo and G B Ramirez-Rodríguez and T Patrício and L D Esposti and F Rossi and F Ravanetti and S Pinelli and R Alinovi and M Erreni and S Rossi and G Condorelli and H Post and A Tampieri and D Catalucci},

year  = {2018},

date = {2018-01-01},

journal = {Sci Transl Med},

volume = {10},

number = {424},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid29513717,

title = {An anti-PĐGFRβ aptamer for selective delivery of small therapeutic peptide to cardiac cells},

author = {A Romanelli and A Affinito and C Avitabile and S Catuogno and P Ceriotti and M Iaboni and J Modica and G Condorelli and D Catalucci},

year  = {2018},

date = {2018-01-01},

journal = {PLoS One},

volume = {13},

number = {3},

pages = {e0193392},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid29997259,

title = {A combined low-frequency electromagnetic and fluidic stimulation for a controlled drug release from superparamagnetic calcium phosphate nanoparticles: potential application for cardiovascular diseases},

author = {A Marrella and M Iafisco and A Adamiano and S Rossi and M Aiello and M Barandalla-Sobrados and P Carullo and M Miragoli and A Tampieri and S Scaglione and D Catalucci},

year  = {2018},

date = {2018-01-01},

journal = {J R Soc Interface},

volume = {15},

number = {144},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{kallikourdis_t_2017,

title = {T cell costimulation blockade blunts pressure overload-induced heart failure},

author = {Marinos Kallikourdis and Elisa Martini and Pierluigi Carullo and Claudia Sardi and Giuliana Roselli and Carolina M Greco and Debora Vignali and Federica Riva and Anne Marie {Ormbostad Berre} and Tomas O St{ø}len and Andrea Fumero and Giuseppe Faggian and Elisa {Di Pasquale} and Leonardo Elia and Cristiano Rumio and Daniele Catalucci and Roberto Papait and Gianluigi Condorelli},

doi = {10.1038/ncomms14680},

issn = {2041-1723},

year  = {2017},

date = {2017-03-01},

journal = {Nature Communications},

volume = {8},

pages = {14680},

abstract = {Heart failure (HF) is a leading cause of mortality. Inflammation is implicated in HF, yet clinical trials targeting pro-inflammatory cytokines in HF were unsuccessful, possibly due to redundant functions of individual cytokines. Searching for better cardiac inflammation targets, here we link T cells with HF development in a mouse model of pathological cardiac hypertrophy and in human HF patients. T cell costimulation blockade, through FDA-approved rheumatoid arthritis drug abatacept, leads to highly significant delay in progression and decreased severity of cardiac dysfunction in the mouse HF model. The therapeutic effect occurs via inhibition of activation and cardiac infiltration of T cells and macrophages, leading to reduced cardiomyocyte death. Abatacept treatment also induces production of anti-inflammatory cytokine interleukin-10 (IL-10). IL-10-deficient mice are refractive to treatment, while protection could be rescued by transfer of IL-10-sufficient B cells. These results suggest that T cell costimulation blockade might be therapeutically exploited to treat HF.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid29073097,

title = {Content of mitochondrial calcium uniporter (MCU) in cardiomyocytes is regulated by microRNA-1 in physiologic and pathologic hypertrophy},

author = {T Zaglia and P Ceriotti and A Campo and G Borile and A Armani and P Carullo and V Prando and R Coppini and V Vida and T O Stølen and W Ulrik and E Cerbai and G Stellin and G Faggian and D De Stefani and M Sandri and R Rizzuto and F Di Lisa and T Pozzan and D Catalucci and M Mongillo},

year  = {2017},

date = {2017-01-01},

journal = {Proc Natl Acad Sci U S A},

volume = {114},

number = {43},

pages = {E9006-E9015},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{rusconi_peptidomimetic_2016,

title = {Peptidomimetic Targeting of Cavβ2 Overcomes Dysregulation of the L-Type Calcium Channel Density and Recovers Cardiac Function},

author = {Francesca Rusconi and Paola Ceriotti and Michele Miragoli and Pierluigi Carullo and Nicol{ò} Salvarani and Marcella Rocchetti and Elisa {Di Pasquale} and Stefano Rossi and Maddalena Tessari and Silvia Caprari and Magali Cazade and Paolo Kunderfranco and Jean Chemin and Marie-Louise Bang and Fabio Polticelli and Antonio Zaza and Giuseppe Faggian and Gianluigi Condorelli and Daniele Catalucci},

doi = {10.1161/CIRCULATIONAHA.116.021347},

issn = {1524-4539},

year  = {2016},

date = {2016-08-01},

journal = {Circulation},

volume = {134},

number = {7},

pages = {534--546},

abstract = {BACKGROUND: L-type calcium channels (LTCCs) play important roles in regulating cardiomyocyte physiology, which is governed by appropriate LTCC trafficking to and density at the cell surface. Factors influencing the expression, half-life, subcellular trafficking, and gating of LTCCs are therefore critically involved in conditions of cardiac physiology and disease. 

METHODS: Yeast 2-hybrid screenings, biochemical and molecular evaluations, protein interaction assays, fluorescence microscopy, structural molecular modeling, and functional studies were used to investigate the molecular mechanisms through which the LTCC Cavβ2 chaperone regulates channel density at the plasma membrane. 

RESULTS: On the basis of our previous results, we found a direct linear correlation between the total amount of the LTCC pore-forming Cavα1.2 and the Akt-dependent phosphorylation status of Cavβ2 both in a mouse model of diabetic cardiac disease and in 6 diabetic and 7 nondiabetic cardiomyopathy patients with aortic stenosis undergoing aortic valve replacement. Mechanistically, we demonstrate that a conformational change in Cavβ2 triggered by Akt phosphorylation increases LTCC density at the cardiac plasma membrane, and thus the inward calcium current, through a complex pathway involving reduction of Cavα1.2 retrograde trafficking and protein degradation through the prevention of dynamin-mediated LTCC endocytosis; promotion of Cavα1.2 anterograde trafficking by blocking Kir/Gem-dependent sequestration of Cavβ2, thus facilitating the chaperoning of Cavα1.2; and promotion of Cavα1.2 transcription by the prevention of Kir/Gem-mediated shuttling of Cavβ2 to the nucleus, where it limits the transcription of Cavα1.2 through recruitment of the heterochromatin protein 1γ epigenetic repressor to the Cacna1c promoter. On the basis of this mechanism, we developed a novel mimetic peptide that, through targeting of Cavβ2, corrects LTCC life-cycle alterations, facilitating the proper function of cardiac cells. Delivery of mimetic peptide into a mouse model of diabetic cardiac disease associated with LTCC abnormalities restored impaired calcium balance and recovered cardiac function. 

CONCLUSIONS: We have uncovered novel mechanisms modulating LTCC trafficking and life cycle and provide proof of concept for the use of Cavβ2 mimetic peptide as a novel therapeutic tool for the improvement of cardiac conditions correlated with alterations in LTCC levels and function.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{di_mauro_bioinspired_2016,

title = {Bioinspired negatively charged calcium phosphate nanocarriers for cardiac delivery of MicroRNAs},

author = {Vittoria {Di Mauro} and Michele Iafisco and Nicol{ò} Salvarani and Marco Vacchiano and Pierluigi Carullo and Gloria Bel{é}n Ram{í}rez-Rodr{í}guez and Tatiana Patr{í}cio and Anna Tampieri and Michele Miragoli and Daniele Catalucci},

doi = {10.2217/nnm.16.26},

issn = {1748-6963},

year  = {2016},

date = {2016-04-01},

journal = {Nanomedicine (London, England)},

volume = {11},

number = {8},

pages = {891--906},

abstract = {AIM: To develop biocompatible and bioresorbable negatively charged calcium phosphate nanoparticles (CaP-NPs) as an innovative therapeutic system for the delivery of bioactive molecules to the heart. 

MATERIALS & METHODS: CaP-NPs were synthesized via a straightforward one-pot biomineralization-inspired protocol employing citrate as a stabilizing agent and regulator of crystal growth. CaP-NPs were administered to cardiac cells in vitro and effects of treatments were assessed. CaP-NPs were administered in vivo and delivery of microRNAs was evaluated. 

RESULTS: CaP-NPs efficiently internalized into cardiomyocytes without promoting toxicity or interfering with any functional properties. CaP-NPs successfully encapsulated synthetic microRNAs, which were efficiently delivered into cardiac cells in vitro and in vivo. 

CONCLUSION: CaP-NPs are a safe and efficient drug-delivery system for potential therapeutic treatments of polarized cells such as cardiomyocytes.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid26214837,

title = {Neutrophils promote Alzheimer's disease-like pathology and cognitive decline via LFA-1 integrin},

author = {E Zenaro and E Pietronigro and V Della Bianca and G Piacentino and L Marongiu and S Budui and E Turano and B Rossi and S Angiari and S Dusi and A Montresor and T Carlucci and S Nanì and G Tosadori and L Calciano and D Catalucci and G Berton and B Bonetti and G Constantin},

year  = {2015},

date = {2015-01-01},

journal = {Nat Med},

volume = {21},

number = {8},

pages = {880--886},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{castaldi_microrna-133_2014,

title = {MicroRNA-133 modulates the β1-adrenergic receptor transduction cascade},

author = {Alessandra Castaldi and Tania Zaglia and Vittoria {Di Mauro} and Pierluigi Carullo and Giacomo Viggiani and Giulia Borile and Barbara {Di Stefano} and Gabriele Giacomo Schiattarella and Maria Giovanna Gualazzi and Leonardo Elia and Giuliano Giuseppe Stirparo and Maria Luisa Colorito and Gianluigi Pironti and Paolo Kunderfranco and Giovanni Esposito and Marie-Louise Bang and Marco Mongillo and Gianluigi Condorelli and Daniele Catalucci},

doi = {10.1161/CIRCRESAHA.115.303252},

issn = {1524-4571},

year  = {2014},

date = {2014-07-01},

journal = {Circulation Research},

volume = {115},

number = {2},

pages = {273--283},

abstract = {RATIONALE: The sympathetic nervous system plays a fundamental role in the regulation of myocardial function. During chronic pressure overload, overactivation of the sympathetic nervous system induces the release of catecholamines, which activate β-adrenergic receptors in cardiomyocytes and lead to increased heart rate and cardiac contractility. However, chronic stimulation of β-adrenergic receptors leads to impaired cardiac function, and β-blockers are widely used as therapeutic agents for the treatment of cardiac disease. MicroRNA-133 (miR-133) is highly expressed in the myocardium and is involved in controlling cardiac function through regulation of messenger RNA translation/stability. 

OBJECTIVE: To determine whether miR-133 affects β-adrenergic receptor signaling during progression to heart failure. 

METHODS AND RESULTS: Based on bioinformatic analysis, β1-adrenergic receptor (β1AR) and other components of the β1AR signal transduction cascade, including adenylate cyclase VI and the catalytic subunit of the cAMP-dependent protein kinase A, were predicted as direct targets of miR-133 and subsequently validated by experimental studies. Consistently, cAMP accumulation and activation of downstream targets were repressed by miR-133 overexpression in both neonatal and adult cardiomyocytes following selective β1AR stimulation. Furthermore, gain-of-function and loss-of-function studies of miR-133 revealed its role in counteracting the deleterious apoptotic effects caused by chronic β1AR stimulation. This was confirmed in vivo using a novel cardiac-specific TetON-miR-133 inducible transgenic mouse model. When subjected to transaortic constriction, TetON-miR-133 inducible transgenic mice maintained cardiac performance and showed attenuated apoptosis and reduced fibrosis compared with control mice. 

CONCLUSIONS: miR-133 controls multiple components of the β1AR transduction cascade and is cardioprotective during heart failure.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{zaglia_atrogin-1_2014,

title = {Atrogin-1 deficiency promotes cardiomyopathy and premature death via impaired autophagy},

author = {Tania Zaglia and Giulia Milan and Aaron Ruhs and Mauro Franzoso and Enrico Bertaggia and Nicola Pianca and Andrea Carpi and Pierluigi Carullo and Paola Pesce and David Sacerdoti and Cristiano Sarais and Daniele Catalucci and Marcus Kr{ü}ger and Marco Mongillo and Marco Sandri},

doi = {10.1172/JCI66339},

issn = {1558-8238},

year  = {2014},

date = {2014-06-01},

journal = {The Journal of Clinical Investigation},

volume = {124},

number = {6},

pages = {2410--2424},

abstract = {Cardiomyocyte proteostasis is mediated by the ubiquitin/proteasome system (UPS) and autophagy/lysosome system and is fundamental for cardiac adaptation to both physiologic (e.g., exercise) and pathologic (e.g., pressure overload) stresses. Both the UPS and autophagy/lysosome system exhibit reduced efficiency as a consequence of aging, and dysfunction in these systems is associated with cardiomyopathies. The muscle-specific ubiquitin ligase atrogin-1 targets signaling proteins involved in cardiac hypertrophy for degradation. Here, using atrogin-1 KO mice in combination with in vivo pulsed stable isotope labeling of amino acids in cell culture proteomics and biochemical and cellular analyses, we identified charged multivesicular body protein 2B (CHMP2B), which is part of an endosomal sorting complex (ESCRT) required for autophagy, as a target of atrogin-1-mediated degradation. Mice lacking atrogin-1 failed to degrade CHMP2B, resulting in autophagy impairment, intracellular protein aggregate accumulation, unfolded protein response activation, and subsequent cardiomyocyte apoptosis, all of which increased progressively with age. Cellular proteostasis alterations resulted in cardiomyopathy characterized by myocardial remodeling with interstitial fibrosis, with reduced diastolic function and arrhythmias. CHMP2B downregulation in atrogin-1 KO mice restored autophagy and decreased proteotoxicity, thereby preventing cell death. These data indicate that atrogin-1 promotes cardiomyocyte health through mediating the interplay between UPS and autophagy/lysosome system and its alteration promotes development of cardiomyopathies.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid23436819,

title = {An SRF/miR-1 axis regulates NCX1 and annexin A5 protein levels in the normal and failing heart},

author = {E Tritsch and Y Mallat and F Lefebvre and N Diguet and B Escoubet and J Blanc and L J De Windt and D Catalucci and G Vandecasteele and Z Li and M Mericskay},

year  = {2013},

date = {2013-06-01},

journal = {Cardiovasc Res},

volume = {98},

number = {3},

pages = {372--380},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{varrone_circulating_2013,

title = {The circulating level of FABP3 is an indirect biomarker of microRNA-1},

author = {Francesca Varrone and Barbara Gargano and Pierluigi Carullo and Dario {Di Silvestre} and Antonella {De Palma} and Ludovica Grasso and Carolina {Di Somma} and Pierluigi Mauri and Louise Benazzi and Anna Franzone and Gloria Saccani Jotti and Marie-Louise Bang and Giovanni Esposito and Annamaria Colao and Gianluigi Condorelli and Daniele Catalucci},

doi = {10.1016/j.jacc.2012.08.1003},

issn = {1558-3597},

year  = {2013},

date = {2013-01-01},

journal = {Journal of the American College of Cardiology},

volume = {61},

number = {1},

pages = {88--95},

abstract = {OBJECTIVES: This study sought to identify proteins from the cardiomyocyte (CM) secretome that are directly targeted by the muscle-specific microRNA-1 (miR-1), and thus reflect the pathophysiological state of the CM. 

BACKGROUND: MicroRNAs play critical regulatory roles during myocardial remodeling and progression to heart failure. However, it remains unknown whether secreted microRNA-targeted proteins can be used as indicators of myocardial microRNA expression and function. 

METHODS: A proteomic analysis based on multidimensional protein identification technology was performed on supernatants from cultured CMs overexpressing miR-1. Biochemical assays and an inducible cardiac-specific transgenic mouse model overexpressing miR-1 were used to demonstrate that heart-type fatty acid-binding protein-3 (FABP3) is a target of miR-1. Levels of miR-1 and FABP3 in cardiac tissue and plasma samples from mouse models as well as human patients were quantified by quantitative reverse-transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The study included wild-type mice subjected to ventricular pressure overload or fasting, as well as patients diagnosed with ventricular hypertrophy due to valvular aortic stenosis, acromegaly, or growth hormone deficiency, conditions associated with altered miR-1 expression. 

RESULTS: An inverse relationship between myocardial expression of miR-1 and circulating levels of FABP3 was found both in vitro and in vivo under various pathological conditions. 

CONCLUSIONS: Assessment of FABP3 plasma levels in human patients might be used for indirectly measuring cardiac miR-1 activity.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid23922949,

title = {MicroRNA-1 downregulation increases connexin 43 displacement and induces ventricular tachyarrhythmias in rodent hypertrophic hearts},

author = {A Curcio and D Torella and C Iaconetti and E Pasceri and J Sabatino and S Sorrentino and S Giampà and M Micieli and A Polimeni and B J Henning and A Leone and D Catalucci and G M Ellison and G Condorelli and C Indolfi},

year  = {2013},

date = {2013-01-01},

journal = {PLoS One},

volume = {8},

number = {7},

pages = {e70158},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid23166348,

title = {Mutual antagonism between IP(3)RII and miRNA-133a regulates calcium signals and cardiac hypertrophy},

author = {F M Drawnel and D Wachten and J D Molkentin and M Maillet and J M Aronsen and F Swift and I Sjaastad and N Liu and D Catalucci and K Mikoshiba and C Hisatsune and H Okkenhaug and S R Andrews and M D Bootman and H L Roderick},

year  = {2012},

date = {2012-11-01},

journal = {J Cell Biol},

volume = {199},

number = {5},

pages = {783--798},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid21769867,

title = {MiR-133a regulates collagen 1A1: potential role of miR-133a in myocardial fibrosis in angiotensin II-dependent hypertension},

author = {G Castoldi and C R Di Gioia and C Bombardi and D Catalucci and B Corradi and M G Gualazzi and M Leopizzi and M Mancini and G Zerbini and G Condorelli and A Stella},

year  = {2012},

date = {2012-02-01},

journal = {J Cell Physiol},

volume = {227},

number = {2},

pages = {850--856},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid22810587,

title = {APJ acts as a dual receptor in cardiac hypertrophy},

author = {M C Scimia and C Hurtado and S Ray and S Metzler and K Wei and J Wang and C E Woods and N H Purcell and D Catalucci and T Akasaka and O F Bueno and G P Vlasuk and P Kaliman and R Bodmer and L H Smith and E Ashley and M Mercola and J H Brown and P Ruiz-Lozano},

year  = {2012},

date = {2012-01-01},

journal = {Nature},

volume = {488},

number = {7411},

pages = {394--398},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid21852550,

title = {MicroRNA-133 controls vascular smooth muscle cell phenotypic switch in vitro and vascular remodeling in vivo},

author = {D Torella and C Iaconetti and D Catalucci and G M Ellison and A Leone and C D Waring and A Bochicchio and C Vicinanza and I Aquila and A Curcio and G Condorelli and C Indolfi},

year  = {2011},

date = {2011-09-01},

journal = {Circ Res},

volume = {109},

number = {8},

pages = {880--893},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid21598388,

title = {A comparative MudPIŦ analysis identifies different expression profiles in heart compartments},

author = {C Comunian and F Rusconi and A De Palma and P Brunetti and D Catalucci and P L Mauri},

year  = {2011},

date = {2011-06-01},

journal = {Proteomics},

volume = {11},

number = {11},

pages = {2320--2328},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid20644257,

title = {MŦORC1 regulates cardiac function and myocyte survival through 4E-BP1 inhibition in mice},

author = {D Zhang and R Contu and M V Latronico and J Zhang and J L Zhang and R Rizzi and D Catalucci and S Miyamoto and K Huang and M Ceci and Y Gu and N D Dalton and K L Peterson and K L Guan and J H Brown and J Chen and N Sonenberg and G Condorelli},

year  = {2010},

date = {2010-01-01},

journal = {J Clin Invest},

volume = {120},

number = {8},

pages = {2805--2816},

keywords = {},

pubstate = {published},

tppubtype = {article}

}