Elisa Di Pasquale

@article{pmid32719615,

title = {Ŧhe Broad Spectrum of LMNA Cardiac Điseases: From Molecular Mechanisms to Clinical Phenotype},

author = {S Crasto and I My and E Di Pasquale},

year  = {2020},

date = {2020-01-01},

journal = {Front Physiol},

volume = {11},

pages = {761},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid32528940,

title = {Ŧoward Cardiac Regeneration: Combination of Pluripotent Stem Cell-Based Ŧherapies and Bioengineering Strategies},

author = {M Mazzola and E Di Pasquale},

year  = {2020},

date = {2020-01-01},

journal = {Front Bioeng Biotechnol},

volume = {8},

pages = {455},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid31066237,

title = {Optical Pacing of Ħuman-Induced Pluripotent Stem Cell-Đerived Cardiomyocytes Mediated by a Conjugated Polymer Interface},

author = {F Lodola and V Vurro and S Crasto and E Di Pasquale and G Lanzani},

year  = {2019},

date = {2019-01-01},

volume = {8},

number = {13},

pages = {e1900198},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid31118417,

title = {Ŧhe K219Ŧ-Lamin mutation induces conduction defects through epigenetic inhibition of SCN5A in human cardiac laminopathy},

author = {N Salvarani and S Crasto and M Miragoli and A Bertero and M Paulis and P Kunderfranco and S Serio and A Forni and C Lucarelli and M Dal Ferro and V Larcher and G Sinagra and P Vezzoni and C E Murry and G Faggian and G Condorelli and E Di Pasquale},

year  = {2019},

date = {2019-01-01},

journal = {Nat Commun},

volume = {10},

number = {1},

pages = {2267},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid30902910,

title = {Endoplasmic reticulum stress at the crossroads of progeria and atherosclerosis},

author = {E Di Pasquale and G Condorelli},

year  = {2019},

date = {2019-01-01},

journal = {EMBO Mol Med},

volume = {11},

number = {4},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid30619852,

title = {Induced Pluripotent Stem Cells to Study Mechanisms of Laminopathies: Focus on Epigenetics},

author = {S Crasto and E Di Pasquale},

year  = {2018},

date = {2018-01-01},

journal = {Front Cell Dev Biol},

volume = {6},

pages = {172},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid29878125,

title = {Cofilin-1 phosphorylation catalyzed by ERK1/2 alters cardiac actin dynamics in dilated cardiomyopathy caused by lamin A/C gene mutation},

author = {M Chatzifrangkeskou and D Yadin and T Marais and S Chardonnet and M Cohen-Tannoudji and N Mougenot and A Schmitt and S Crasto and E Di Pasquale and C Macquart and Y Tanguy and I Jebeniani and M Pucéat and B Morales Rodriguez and W H Goldmann and M Dal Ferro and M G Biferi and P Knaus and G Bonne and H J Worman and A Muchir},

year  = {2018},

date = {2018-01-01},

journal = {Hum Mol Genet},

volume = {27},

number = {17},

pages = {3060--3078},

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{lodola_adeno-associated_2016,

title = {Adeno-associated virus-mediated CASQ2 delivery rescues phenotypic alterations in a patient-specific model of recessive catecholaminergic polymorphic ventricular tachycardia},

author = {Francesco Lodola and Diego Morone and Marco Denegri and Rossana Bongianino and Hiroko Nakahama and Lucia Rutigliano and Rosanna Gosetti and Giulia Rizzo and Alessandra Vollero and Michelangelo Buonocore and Carlo Napolitano and Gianluigi Condorelli and Silvia G Priori and Elisa {Di Pasquale}},

doi = {10.1038/cddis.2016.304},

issn = {2041-4889},

year  = {2016},

date = {2016-10-01},

journal = {Cell Death & Disease},

volume = {7},

number = {10},

pages = {e2393},

abstract = {Catecholaminergic Polymorphic Ventricular Tachycardia type 2 (CPVT2) is a highly lethal recessive arrhythmogenic disease caused by mutations in the calsequestrin-2 (CASQ2) gene. We have previously demonstrated that viral transfer of the wild-type (WT) CASQ2 gene prevents the development of CPVT2 in a genetically induced mouse model of the disease homozygous carrier of the R33Q mutation. In the present study, we investigated the efficacy of the virally mediated gene therapy in cardiomyocytes (CMs) differentiated from induced pluripotent stem cells (iPSCs) obtained from a patient carrying the homozygous CASQ2-G112+5X mutation. To this end, we infected cells with an Adeno-Associated Viral vector serotype 9 (AAV9) encoding the human CASQ2 gene (AAV9-hCASQ2). Administration of the human WT CASQ2 gene was capable and sufficient to restore the physiological expression of calsequestrin-2 protein and to rescue functional defects of the patient-specific iPSC-derived CMs. Indeed, after viral gene transfer, we observed a remarkable decrease in the percentage of delayed afterdepolarizations (DADs) developed by the diseased CMs upon adrenergic stimulation, the calcium transient amplitude was re-established and the density and duration of calcium sparks were normalized. We therefore demonstrate the efficacy of the AAV9-mediated gene replacement therapy for CPVT2 in a human cardiac-specific model system, supporting the view that the gene-therapy tested is curative in models with different human mutations of CPVT.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{di_pasquale_camkii_2013,

title = {CaMKII inhibition rectifies arrhythmic phenotype in a patient-specific model of catecholaminergic polymorphic ventricular tachycardia},

author = {E {Di Pasquale} and F Lodola and M Miragoli and M Denegri and J E Avelino-Cruz and M Buonocore and H Nakahama and P Portararo and R Bloise and C Napolitano and G Condorelli and S G Priori},

doi = {10.1038/cddis.2013.369},

issn = {2041-4889},

year  = {2013},

date = {2013-10-01},

journal = {Cell Death & Disease},

volume = {4},

pages = {e843},

abstract = {Induced pluripotent stem cells (iPSC) offer a unique opportunity for developmental studies, disease modeling and regenerative medicine approaches in humans. The aim of our study was to create an in vitro 'patient-specific cell-based system' that could facilitate the screening of new therapeutic molecules for the treatment of catecholaminergic polymorphic ventricular tachycardia (CPVT), an inherited form of fatal arrhythmia. Here, we report the development of a cardiac model of CPVT through the generation of iPSC from a CPVT patient carrying a heterozygous mutation in the cardiac ryanodine receptor gene (RyR2) and their subsequent differentiation into cardiomyocytes (CMs). Whole-cell patch-clamp and intracellular electrical recordings of spontaneously beating cells revealed the presence of delayed afterdepolarizations (DADs) in CPVT-CMs, both in resting conditions and after β-adrenergic stimulation, resembling the cardiac phenotype of the patients. Furthermore, treatment with KN-93 (2-[N-(2-hydroxyethyl)]-N-(4methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzylamine), an antiarrhythmic drug that inhibits Ca(2+)/calmodulin-dependent serine-threonine protein kinase II (CaMKII), drastically reduced the presence of DADs in CVPT-CMs, rescuing the arrhythmic phenotype induced by catecholaminergic stress. In addition, intracellular calcium transient measurements on 3D beating clusters by fast resolution optical mapping showed that CPVT clusters developed multiple calcium transients, whereas in the wild-type clusters, only single initiations were detected. Such instability is aggravated in the presence of isoproterenol and is attenuated by KN-93. As seen in our RyR2 knock-in CPVT mice, the antiarrhythmic effect of KN-93 is confirmed in these human iPSC-derived cardiac cells, supporting the role of this in vitro system for drug screening and optimization of clinical treatment strategies.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{priori_induced_2013,

title = {Induced pluripotent stem cell-derived cardiomyocytes in studies of inherited arrhythmias},

author = {Silvia G Priori and Carlo Napolitano and Elisa {Di Pasquale} and Gianluigi Condorelli},

doi = {10.1172/JCI62838},

issn = {1558-8238},

year  = {2013},

date = {2013-01-01},

journal = {The Journal of Clinical Investigation},

volume = {123},

number = {1},

pages = {84--91},

abstract = {The discovery of the genetic basis of inherited arrhythmias has paved the way for an improved understanding of arrhythmogenesis in a wide spectrum of life-threatening conditions. In vitro expression of mutations and transgenic animal models have been instrumental in enhancing this understanding, but the applicability of results to the human heart remains unknown. The ability to differentiate induced pluripotent stem cells (iPSs) into cardiomyocytes enables the potential to generate patient-specific myocytes, which could be used to recapitulate the features of inherited arrhythmias in the context of the patient's genetic background. Few studies have been reported on iPS-derived myocytes obtained from patients with heritable arrhythmias, but they have demonstrated the applicability of this innovative approach to the study of inherited arrhythmias. Here we review the results achieved by iPS investigations in arrhythmogenic syndromes and discuss the existing challenges to be addressed before the use of iPS-derived myocytes can become a part of personalized management of inherited arrhythmias.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{rizzi_post-natal_2012,

title = {Post-natal cardiomyocytes can generate iPS cells with an enhanced capacity toward cardiomyogenic re-differentation},

author = {R Rizzi and E {Di Pasquale} and P Portararo and R Papait and P Cattaneo and M V G Latronico and C Altomare and L Sala and A Zaza and E Hirsch and L Naldini and G Condorelli and C Bearzi},

doi = {10.1038/cdd.2011.205},

issn = {1476-5403},

year  = {2012},

date = {2012-07-01},

journal = {Cell Death and Differentiation},

volume = {19},

number = {7},

pages = {1162--1174},

abstract = {Adult mammalian cells can be reprogrammed to a pluripotent state by forcing the expression of a few embryonic transcription factors. The resulting induced pluripotent stem (iPS) cells can differentiate into cells of all three germ layers. It is well known that post-natal cardiomyocytes (CMs) lack the capacity to proliferate. Here, we report that neonatal CMs can be reprogrammed to generate iPS cells that express embryonic-specific markers and feature gene-expression profiles similar to those of mouse embryonic stem (mES) cell and cardiac fibroblast (CF)-derived iPS cell populations. CM-derived iPS cells are able to generate chimeric mice and, moreover, re-differentiate toward CMs more efficiently then either CF-derived iPS cells or mES cells. The increased differentiation capacity is possibly related to CM-derived iPS cells retaining an epigenetic memory of the phenotype of their founder cell. CM-derived iPS cells may thus lead to new information on differentiation processes underlying cardiac differentiation and proliferation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid19553676,

title = {Bone morphogenetic protein 15 (BMP15) acts as a BMP and Wnt inhibitor during early embryogenesis},

author = {E Di Pasquale and A H Brivanlou},

year  = {2009},

date = {2009-09-01},

journal = {J Biol Chem},

volume = {284},

number = {38},

pages = {26127--26136},

keywords = {},

pubstate = {published},

tppubtype = {article}

}