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Your search keyword '"D'ONOFRIO, NUNZIA"' showing total 9 results
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9 results on '"D'ONOFRIO, NUNZIA"'

3. Does poor glycaemic control affect the immunogenicity of the COVID‐19 vaccination in patients with type 2 diabetes: The CAVEAT study

Author

Marfella, Raffaele, primary, D'Onofrio, Nunzia, additional, Sardu, Celestino, additional, Scisciola, Lucia, additional, Maggi, Paolo, additional, Coppola, Nicola, additional, Romano, Ciro, additional, Messina, Vincenzo, additional, Turriziani, Fabrizio, additional, Siniscalchi, Mario, additional, Maniscalco, Mauro, additional, Boccalatte, Marco, additional, Napolitano, Giovanni, additional, Salemme, Luigi, additional, Marfella, Ludovica Vittoria, additional, Basile, Eugenio, additional, Montemurro, Maria Vittoria, additional, Papa, Carmela, additional, Frascaria, Francesco, additional, Papa, Antonio, additional, Russo, Ferdinando, additional, Tirino, Virginia, additional, Papaccio, Gianpaolo, additional, Galdiero, Marilena, additional, Sasso, Ferdinando Carlo, additional, Barbieri, Michelangela, additional, Rizzo, Maria Rosaria, additional, Balestrieri, Maria Luisa, additional, Angelillo, Italo Francesco, additional, Napoli, Claudio, additional, and Paolisso, Giuseppe, additional

Published
2021
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6. MicroRNA‐33 and SIRT1 influence the coronary thrombus burden in hyperglycemic STEMI patients

Author

D'Onofrio, Nunzia, primary, Sardu, Celestino, additional, Paolisso, Pasquale, additional, Minicucci, Fabio, additional, Gragnano, Felice, additional, Ferraraccio, Franca, additional, Panarese, Iacopo, additional, Scisciola, Lucia, additional, Mauro, Ciro, additional, Rizzo, Maria Rosaria, additional, Mansueto, Gelsomina, additional, Varavallo, Federica, additional, Brunitto, Giuseppina, additional, Caserta, Rosanna, additional, Tirino, Virginia, additional, Papaccio, Gianpaolo, additional, Barbieri, Michelangela, additional, Paolisso, Giuseppe, additional, Balestrieri, Maria Luisa, additional, and Marfella, Raffaele, additional

Published
2019
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8. Incretin drugs effect on epigenetic machinery: New potential therapeutic implications in preventing vascular diabetic complications

Author

Giuseppe Paolisso, Rosaria Anna Fontanella, Michelangela Barbieri, Maria Luisa Balestrieri, Lucia Scisciola, Vittoria Cataldo, Raffaele Marfella, Maria Rosaria Rizzo, Nunzia D'Onofrio, Scisciola, Lucia, Rizzo, Maria Rosaria, Cataldo, Vittoria, Fontanella, Rosaria Anna, Balestrieri, Maria Luisa, D'Onofrio, Nunzia, Marfella, Raffaele, Paolisso, Giuseppe, and Barbieri, Michelangela

Subjects
Blood Glucose, 0301 basic medicine, medicine.medical_specialty, Methyltransferase, SOD2, Gene Expression, Incretin, Type 2 diabetes, Carotid Intima-Media Thickness, Incretins, Biochemistry, Glucagon-Like Peptide-1 Receptor, Body Mass Index, Cell Line, Epigenesis, Genetic, Diabetes Complications, 03 medical and health sciences, incretin based drug, 0302 clinical medicine, Internal medicine, Genetics, Humans, Medicine, Epigenetics, Molecular Biology, Superoxide Dismutase, business.industry, NF-kappa B, Endothelial Cells, Methylation, DNA Methylation, Atherosclerosis, medicine.disease, Glucose, 030104 developmental biology, Endocrinology, Diabetes Mellitus, Type 2, Intima-media thickness, DNA methylation, atherosclerosis progression, cardiovascular system, type 2 diabetes, business, 030217 neurology & neurosurgery, Biotechnology
Abstract

The effect of GLP-1R agonists on DNA methylation levels of NF-κB and SOD2 genes in human aortic endothelial cells exposed to high glucose and in diabetic patients treated and not with incretin-based drugs, was evaluated. Methylation levels, mRNA and protein expression of NF-κB and SOD2 genes were measured in human endothelial cells exposed to high glucose for 7days and treated with GLP-1R agonists. Methylation status of NF-κB and SOD2 promoter was also analyzed in 128 diabetics and 116 nondiabetics and correlated with intima media thickness (ITM), an early marker of atherosclerotic process. Cells exposed to high glucose showed lower NF-κB and SOD2 methylation levels, increased NF-κB and reduced SOD2 expression compared to normal glucose cells. Co-treatment with GLP-1 agonists prevented methylation and genes expression changes induced by high glucose. Both high glucose and incretins exposure increased DNA methyltransferases and demethylases levels. In diabetics, incretin treatment resulted a significant predictor of NF-κB DNA methylation, independently of age, sex, body mass index (BMI), glucose and plasma lipid levels. NF-κB DNA methylation inversely correlated with IMT after adjusting for multiple covariates. Our results firstly provide new evidences of an additional mechanism by which incretin drugs could prevent vascular diabetic complications.

Published
2020

9. MicroRNA‐33 and SIRT1 influence the coronary thrombus burden in hyperglycemic STEMI patients

Author

Iacopo Panarese, Pasquale Paolisso, Michelangela Barbieri, Federica Varavallo, Nunzia D'Onofrio, Maria Luisa Balestrieri, Giuseppina Brunitto, Raffaele Marfella, Maria Rosaria Rizzo, Giuseppe Paolisso, Franca Ferraraccio, Gianpaolo Papaccio, Virginia Tirino, Ciro Mauro, Gelsomina Mansueto, Felice Gragnano, Celestino Sardu, Rosanna Caserta, Fabio Minicucci, Lucia Scisciola, D'Onofrio, Nunzia, Sardu, Celestino, Paolisso, Pasquale, Minicucci, Fabio, Gragnano, Felice, Ferraraccio, Franca, Panarese, Iacopo, Scisciola, Lucia, Mauro, Ciro, Rizzo, Maria Rosaria, Mansueto, Gelsomina, Varavallo, Federica, Brunitto, Giuseppina, Caserta, Rosanna, Tirino, Virginia, Papaccio, Gianpaolo, Barbieri, Michelangela, Paolisso, Giuseppe, Balestrieri, Maria Luisa, and Marfella, Raffaele

Subjects
0301 basic medicine, medicine.medical_specialty, Physiology, medicine.medical_treatment, Clinical Biochemistry, Myocardial Infarction, medicine.disease_cause, Cell Line, Cohort Studies, STEMI, 03 medical and health sciences, SIRT1, 0302 clinical medicine, Sirtuin 1, Coronary thrombus, Internal medicine, microRNA, medicine, Humans, oxidative stress, Gene Silencing, cardiovascular diseases, Myocardial infarction, biology, business.industry, Coronary Thrombosis, Incidence (epidemiology), Causal effect, Endothelial Cells, Percutaneous coronary intervention, Cell Biology, medicine.disease, MicroRNAs, miR33, 030104 developmental biology, 030220 oncology & carcinogenesis, Cardiology, biology.protein, hyperglycemia, business, Oxidative stress
Abstract

Primary percutaneous coronary intervention (PPCI) is a pivotal treatment in ST-segment elevation myocardial infarction (STEMI) patients. However, in hyperglycemic-STEMI patients, the incidence of death is still significant. Here, the involvement of sirtuin 1 (SIRT1) and miR33 on the pro-inflammatory/pro-coagulable state of the coronary thrombus was investigated. Moreover, 1-year outcomes in hyperglycemic STEMI in patients subjected to thrombus aspiration before PPCI were evaluated. Results showed that hyperglycemic thrombi displayed higher size and increased miR33, reactive oxygen species, and pro-inflammatory/pro-coagulable markers. Conversely, the hyperglycemic thrombi showed a lower endothelial SIRT1 expression. Moreover, in vitro experiments on endothelial cells showed a causal effect of SIRT1 modulation on the pro-inflammatory/pro-coagulative state via hyperglycemia-induced miR33 expression. Finally, SIRT1 expression negatively correlated with STEMI outcomes. These observations demonstrate the involvement of the miR33/SIRT1 pathway in the increased pro-inflammatory and pro-coagulable state of coronary thrombi in hyperglycemic STEMI patients.

Published
2019

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