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33 results on '"Arcidiacono, Maria Vittoria"'

1. Barley-ß-glucans reduce systemic inflammation, renal injury and aortic calcification through ADAM17 and neutral-sphingomyelinase2 inhibition

Author

Arcidiacono, Maria Vittoria, Carrillo-López, Natalia, Panizo, Sara, Castro-Grattoni, Anabel L., Valcheva, Petya, Ulloa, Catalina, Rodríguez-Carrio, Javier, Cardús, Anna, Quirós-Caso, Covadonga, Martínez-Arias, Laura, Martínez-Salgado, Carlos, Motilva, María José, Rodriguez-Suarez, Carmen, Cannata-Andía, Jorge B., and Dusso, Adriana S.

Published
2019
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4. Vitamin D Treatment Prevents Uremia-Induced Reductions in Aortic microRNA-145 Attenuating Osteogenic Differentiation despite Hyperphosphatemia

Author

Carrillo-López, Natalia, primary, Panizo, Sara, additional, Arcidiacono, Maria Vittoria, additional, de la Fuente, Sandra, additional, Martínez-Arias, Laura, additional, Ottaviano, Emerenziana, additional, Ulloa, Catalina, additional, Ruiz-Torres, María Piedad, additional, Rodríguez, Isabel, additional, Cannata-Andía, Jorge B., additional, Naves-Díaz, Manuel, additional, and Dusso, Adriana S., additional

Published
2022
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9. Novel Immune Cell Subsets Exhibit Different Associations With Vascular Outcomes in Chronic Kidney Disease Patients—Identifying Potential Biomarkers

Author

Rodríguez-Carrio, Javier, primary, Carrillo-López, Natalia, additional, Ulloa, Catalina, additional, Martín-Carro, Beatriz, additional, Rodríguez-Suárez, Carmen, additional, Naves-Díaz, Manuel, additional, Sánchez-Álvarez, Emilio, additional, Rodríguez-García, Minerva, additional, Arcidiacono, Maria Vittoria, additional, Fernández-Mariño, Belinda, additional, Cannata-Andía, Jorge B., additional, Suárez, Ana, additional, and Dusso, Adriana S., additional

Published
2021
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11. P1292DECREASES IN ANGIOGENIC T CELLS ARE PREDICTIVE BIOMARKERS OF VASCULAR DYSFUNCTION AND ATHEROSCLEROSIS IN CHRONIC KIDNEY DISEASE

Author

Carrillo-Lopez, Natalia, primary, Rodriguez-Carrio, Javier, primary, Ulloa, Catalina, primary, Martín-Carro, Beatriz, primary, Rodriguez-Suarez, Carmen, primary, Arcidiacono, Maria Vittoria, primary, Fernandez-Mariño, Belinda, primary, Cannata-Andia, Jorge B, primary, Suarez, Ana, primary, and Dusso, Adriana S, primary

Published
2020
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15. Relationship between low levels of circulating TRAIL and atheromatosis progression in patients with chronic kidney disease

Author

Arcidiacono, Maria Vittoria, primary, Rimondi, Erika, additional, Maietti, Elisa, additional, Melloni, Elisabetta, additional, Tisato, Veronica, additional, Gallo, Stefania, additional, Valdivielso, Jose Manuel, additional, Fernández, Elvira, additional, Betriu, Àngels, additional, Voltan, Rebecca, additional, Zauli, Giorgio, additional, Volpato, Stefano, additional, and Secchiero, Paola, additional

Published
2018
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17. Upregulation of the alternative splicing factor NOVA2 in colorectal cancer vasculature

Author

Gallo,Stefania, Arcidiacono,Maria Vittoria, Tisato,Veronica, Piva,Roberta, Penolazzi,Letizia, Bosi,Cristina, Feo,Carlo, Gafà ,Roberta, Secchiero,Paola, Gallo,Stefania, Arcidiacono,Maria Vittoria, Tisato,Veronica, Piva,Roberta, Penolazzi,Letizia, Bosi,Cristina, Feo,Carlo, Gafà ,Roberta, and Secchiero,Paola

Abstract

Stefania Gallo,1,* Maria Vittoria Arcidiacono,2,* Veronica Tisato,1 Roberta Piva,3 Letizia Penolazzi,3 Cristina Bosi,1 Carlo V Feo,1 Roberta Gafà,1 Paola Secchiero1 1Department of Morphology, Surgery, Experimental Medicine and LTTA Center, University of Ferrara, Ferrara, Italy; 2Institute for Maternal and Child Health, IRCCS “Burlo Garofolo,” Trieste, Italy; 3Department of Biomedical and Specialty Surgical Sciences, University of Ferrara, Ferrara, Italy *These authors contributed equally to this work Background: Tumor-specific isoforms generated by alternative splicing (AS) are demonstrated to contribute to tumor progression and can represent potential biomarkers. NOVA2 is an AS factor that in physiological conditions regulates endothelial cells’ (ECs) polarity and vessel lumen maturation, likely by mediating AS of apical–basal polarity regulators. However, NOVA2 expression in tumor ECs and its regulation have never been investigated. Methods: To elucidate this, 40 colorectal cancer patients were enrolled and NOVA2 expression was investigated by immunohistochemistry in samples bearing both the normal mucosa and the tumor tissue. Results: NOVA2 was found expressed in ECs of tumor vasculature and, importantly, it was upregulated in tumor ECs with respect to normal mucosa ECs in all cases (P<0.001). The same samples analyzed by immunohistochemistry for the expression HIF1α, a marker of hypoxia, showed a positive and significant association with NOVA2 levels (P=0.045). Of note, NOVA2 was upregulated by hypoxia also in an in vitro ECs model. Conclusion: Our results provide, for the first time, evidence of NOVA2 expression and upregulation in tumor ECs and highlight hypoxia as a potential regulatory factor. These findings open a completely new perspective to study tumor vasculature and to uncover NOVA2 as a potential source of biomarkers and therapeutic targets based on AS isoforms. Keywords: NOVA2, tumor

Published
2018

18. MO053REDUCTIONS IN MICRO RNA-145 NOT ONLY AGGRAVATE HIGH-PHOSPHORUS-DRIVEN CALCIFICATION IN ADVANCED CKD STAGES BUT ALSO COMPROMISE VASCULAR HEALTH IN EARLY UREMIA

Author

Carrillo-López, Natalia, primary, Panizo, Sara, additional, Arcidiacono, Maria Vittoria, additional, de la Fuente, Sandra, additional, Castro-Grattoni, Anabel, additional, Naves, Manuel, additional, Rodríguez, Isabel, additional, Cannata-Andía, Jorge, additional, and Dusso, Adriana, additional

Published
2017
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19. High Levels of Hemoglobin Promote Carotid Adventitial Vasa Vasorum Neoangiogenesis in Chronic Kidney Disease

Author

Arcidiacono, Maria Vittoria, primary, Martinez-Alonso, Montserrat, additional, Belart, Montserrat, additional, Vilar, Ana, additional, Martín, Marisa, additional, Craver, Lourdes, additional, Betriu, Àngels, additional, Mauricio, Dídac, additional, Valdivielso, José Manuel, additional, Fernández, Elvira, additional, and Borràs, Mercè, additional

Published
2017
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22. Increased Burden of Cerebral Small Vessel Disease in Patients With Type 2 Diabetes and Retinopathy

Author

Sanahuja, Jordi, primary, Alonso, Núria, additional, Diez, Javier, additional, Ortega, Emilio, additional, Rubinat, Esther, additional, Traveset, Alícia, additional, Alcubierre, Núria, additional, Betriu, Àngels, additional, Castelblanco, Esmeralda, additional, Hernández, Marta, additional, Purroy, Francisco, additional, Arcidiacono, Maria Vittoria, additional, Jurjo, Carmen, additional, Fernández, Elvira, additional, Puig-Domingo, Manuel, additional, Groop, Per-Henrik, additional, and Mauricio, Dídac, additional

Published
2016
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26. Carbamazepin antagonizes the vitamin D-mediated suppression of secondary hyperparathyroidism: Pathogenesis and therapeutical options

Author

Dusso, Adriana, Arcidiacono, Maria Vittoria, Dusso, Adriana, and Arcidiacono, Maria Vittoria

Abstract

Si presenta un aggiornamento su: 1) la fisiopatologia della resistenza indotta dalla carbamazepina all'azione soppressiva del paracalcitolo nell'iperparatiroidismo secondario (IPTS) a malattia renale cronica (CKD); 2) l'impatto di una deficienza di vitamina D sugli effetti indesiderati della carbamazepina; 3) i benefici della supplementazione con colecalciferolo – sia da solo che in associazione con il paracalcitolo – nella prevenzione/attenuazione della soppressione dell'IPTS vitamina D-mediata; 4) la correzione appropriata della carenza di vitamina D nei pazienti con CKD in terapia antiepilettica con carbamazepina, con lo scopo di fornire al nefrologo clinico un approccio terapeutico pratico, sicuro ed efficace, per migliorare l'outcome dell'IPTS., This commentary updates: 1) the patophisiology responsible for carbamazepine-induced resistance to paricalcitol suppression of PTH in CKD; 2) the contribution of vitamin D deficiency to the adverse effects of carbamazepine; 3) the benefits of cholecalciferol supplementation either alone or in combination with paricalcitol in preventing/attenuating the onset of resistance to vitamin D suppression of secondary hyperparathyroidism (SHPT); 4) the successful correction of vitamin D deficiency in chronic kidney disease (CKD) patients receiving anti-epileptic medication other than carbamazepine, with the goal of providing nephrologists with a practical, safe and efficacious therapeutic approach to improve outcomes in SHPT.

Published
2014

32. Ibrutinib synergizes with MDM-2 inhibitors in promoting cytotoxicity in B chronic lymphocytic leukemia

Author

Antonio Cuneo, Claudio Celeghini, Erika Rimondi, Elisabetta Melloni, Rebecca Voltan, Paola Secchiero, Maria Vittoria Arcidiacono, Gian Matteo Rigolin, Giorgio Zauli, Fabio Casciano, Voltan, Rebecca, Rimondi, Erika, Melloni, Elisabetta, Rigolin, Gian Matteo, Casciano, Fabio, Arcidiacono, Maria Vittoria, Celeghini, Claudio, Cuneo, Antonio, Zauli, Giorgio, and Secchiero, Paola

Subjects
0301 basic medicine, MAPK/ERK pathway, Apoptosis, Mice, SCID, Pharmacology, B leukemic cells, Piperazines, MDM-2 inhibitor, combination therapy, chemistry.chemical_compound, 0302 clinical medicine, Piperidines, Antineoplastic Combined Chemotherapy Protocols, MDM-2 inhibitors, Hematology, biology, Ibrutinib, Imidazoles, Drug Synergism, Proto-Oncogene Proteins c-mdm2, Leukemia, Oncology, 030220 oncology & carcinogenesis, Female, apoptosis, Research Paper, medicine.medical_specialty, Combination therapy, Cell Survival, NO, 03 medical and health sciences, Internal medicine, Cell Line, Tumor, medicine, Bruton's tyrosine kinase, Animals, Humans, PI3K/AKT/mTOR pathway, B leukemic cells, Ibrutinib, MDM-2 inhibitors, apoptosis, combination therapy, business.industry, Adenine, medicine.disease, apoptosi, Leukemia, Lymphocytic, Chronic, B-Cell, Xenograft Model Antitumor Assays, 030104 developmental biology, Pyrimidines, chemistry, B leukemic cell, Mutation, biology.protein, Pyrazoles, Tumor Suppressor Protein p53, business
Abstract

// Rebecca Voltan 1, * , Erika Rimondi 2, * , Elisabetta Melloni 1 , Gian Matteo Rigolin 3 , Fabio Casciano 1 , Maria Vittoria Arcidiacono 1 , Claudio Celeghini 2 , Antonio Cuneo 3 , Giorgio Zauli 1 , Paola Secchiero 1 1 Department of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, Italy 2 Department of Life Sciences, University of Trieste, Trieste, Italy 3 Department of Medical Sciences, Section of Hematology, University of Ferrara, Ferrara, Italy * These authors have contributed equally to this work Correspondence to: Paola Secchiero, email: paola.secchiero@unife.it Keywords: B leukemic cells, Ibrutinib, MDM-2 inhibitors, apoptosis, combination therapy Received: July 20, 2016 Accepted: September 09, 2016 Published: September 20, 2016 ABSTRACT Objective: The aim of this study was to investigate the anti-leukemic activity of the Bruton tyrosine kinase inhibitor Ibrutinib in combination with the small molecule MDM-2 inhibitor Nutlin-3 in preclinical models. Methods: The potential efficacy of the Ibrutinib/Nutlin-3 combination was evaluated in vitro in a panel of B leukemic cell lines (EHEB, JVM-2, JVM-3, MEC-1, MEC-2) and in primary B-chronic lymphocytic leukemia (B-CLL) patient samples, by assessing cell viability, cell cycle profile, apoptosis and intracellular pathway modulations. Validation of the combination therapy was assessed in a B leukemic xenograft mouse model. Results: Ibrutinib exhibited variable anti-leukemic activity in vitro and the combination with Nutlin-3 synergistically enhanced the induction of apoptosis independently from the p53 status. Indeed, the Ibrutinib/Nutlin-3 combination was effective in promoting cytotoxicity also in primary B-CLL samples carrying 17p13 deletion and/or TP53 mutations, already in therapy with Ibrutinib. Molecular analyses performed on both B-leukemic cell lines as well as on primary B-CLL samples, while confirming the switch-off of the MAPK and PI3K pro-survival pathways by Ibrutinib, indicated that the synergism of action with Nutlin-3 was independent by p53 pathway and was accompanied by the activation of the DNA damage cascade signaling through the phosphorylation of the histone protein H2A.X. This observation was confirmed also in the JVM-2 B leukemic xenograft mouse model. Conclusions: Taken together, our data emphasize that the Ibrutinib/Nutlin-3 combination merits to be further evaluated as a therapeutic option for B-CLL.

Published
2016

33. Activator protein 2alpha mediates parathyroid TGF-alpha self-induction in secondary hyperparathyroidism.

Author

Arcidiacono MV, Cozzolino M, Spiegel N, Tokumoto M, Yang J, Lu Y, Sato T, Lomonte C, Basile C, Slatopolsky E, and Dusso AS

Subjects
Animals, Case-Control Studies, Female, Humans, Hyperparathyroidism, Secondary pathology, Hyperplasia etiology, Hyperplasia metabolism, Hyperplasia pathology, Parathyroid Glands pathology, Rats, Rats, Sprague-Dawley, Severity of Illness Index, Uremia complications, Uremia pathology, Hyperparathyroidism, Secondary etiology, Hyperparathyroidism, Secondary metabolism, Parathyroid Glands metabolism, Transcription Factor AP-2 metabolism, Transforming Growth Factor alpha physiology, Uremia metabolism
Abstract

In secondary hyperparathyroidism, enhanced expression of TGF-alpha in the parathyroid leads to its own upregulation, generating a feed-forward loop for TGF-alpha activation of its receptor, EGFR receptor (EGFR), which promotes parathyroid hyperplasia. These studies examined the role of activator protein 2alpha (AP2), an inducer of TGF-alpha gene transcription, in the upregulation of parathyroid TGF-alpha in secondary hyperparathyroidism. In rat and human secondary hyperparathyroidism, parathyroid AP2 expression strongly correlated with TGF-alpha levels and with the rate of parathyroid growth, as expected. Furthermore, the increases in rat parathyroid content of AP2 and its binding to a consensus AP2 DNA sequence preceded the increase in TGF-alpha induced by high dietary phosphate. More significant, in A431 cells, which provide a model of enhanced TGF-alpha and TGF-alpha self-induction, mutating the core AP2 site of the human TGF-alpha promoter markedly impaired promoter activity induced by endogenous or exogenous TGF-alpha. Important for therapy, in five-sixths nephrectomized rats fed high-phosphate diets, inhibition of parathyroid TGF-alpha self-induction using erlotinib, a highly specific inhibitor of TGF-alpha/EGFR-driven signals, reduced AP2 expression dosage dependently. This suggests that the increases in parathyroid AP2 occur downstream of EGFR activation by TGF-alpha and are required for TGF-alpha self-induction. Indeed, in A431 cells, erlotinib inhibition of TGF-alpha self-induction caused parallel reductions in AP2 expression and nuclear localization, as well as TGF-alpha mRNA and protein levels. In summary, increased AP2 expression and transcriptional activity at the TGF-alpha promoter determine the severity of the hyperplasia driven by parathyroid TGF-alpha self-upregulation in secondary hyperparathyroidism.

Published
2008
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