Search

Your search keyword '"Zaccagnini, Germana"' showing total 7 results
Start Over Author "Zaccagnini, Germana" Publisher wiley
7 results on '"Zaccagnini, Germana"'

1. P300/CBP‐associated factor regulates transcription and function of isocitrate dehydrogenase 2 during muscle differentiation

Author

Savoia, Matteo, primary, Cencioni, Chiara, additional, Mori, Mattia, additional, Atlante, Sandra, additional, Zaccagnini, Germana, additional, Devanna, Paolo, additional, Di Marcotullio, Lucia, additional, Botta, Bruno, additional, Martelli, Fabio, additional, Zeiher, Andreas M., additional, Pontecorvi, Alfredo, additional, Farsetti, Antonella, additional, Spallotta, Francesco, additional, and Gaetano, Carlo, additional

Published
2018
Full Text
View/download PDF

2. GMP-based CD133+ cells isolation maintains progenitor angiogenic properties and enhances standardization in cardiovascular cell therapy

Author

Gaipa, Giuseppe, primary, Tilenni, Manuela, additional, Straino, Stefania, additional, Burba, Ilaria, additional, Zaccagnini, Germana, additional, Belotti, Daniela, additional, Biagi, Ettore, additional, Valentini, Marco, additional, Perseghin, Paolo, additional, Parma, Matteo, additional, Campli, Cristiana Di, additional, Biondi, Andrea, additional, Capogrossi, Maurizio C., additional, Pompilio, Giulio, additional, and Pesce, Maurizio, additional

Published
2009
Full Text
View/download PDF

3. Common micro‐RNA signature in skeletal muscle damage and regeneration induced by Duchenne muscular dystrophy and acute ischemia

Author

Greco, Simona, primary, De Simone, Marco, additional, Colussi, Claudia, additional, Zaccagnini, Germana, additional, Fasanaro, Pasquale, additional, Pescatori, Mario, additional, Cardani, Rosanna, additional, Perbellini, Riccardo, additional, Isaia, Eleonora, additional, Sale, Patrizio, additional, Meola, Giovanni, additional, Capogrossi, Maurizio C., additional, Gaetano, Carlo, additional, and Martelli, Fabio, additional

Published
2009
Full Text
View/download PDF

5. DNA dose and sequence dependence in sperm-mediated gene transfer

Author

Sciamanna, Ilaria, primary, Piccoli, Simona, additional, Barberi, Laura, additional, Zaccagnini, Germana, additional, Magnano, Anna Rosa, additional, Giordano, Roberto, additional, Campedelli, Paolo, additional, Hodgson, Clague, additional, Lorenzini, Rodolfo, additional, and Spadafora, Corrado, additional

Published
2000
Full Text
View/download PDF

7. miR-210 as a therapeutic target in diabetes-associated endothelial dysfunction.

Author

Collado A, Jiao T, Kontidou E, Carvalho LRRA, Chernogubova E, Yang J, Zaccagnini G, Zhao A, Tengbom J, Zheng X, Rethi B, Alvarsson M, Catrina SB, Mahdi A, Carlström M, Martelli F, Pernow J, and Zhou Z

Abstract

Background and Purpose: MicroRNA (miR)-210 function in endothelial cells and its role in diabetes-associated endothelial dysfunction are not fully understood. We aimed to characterize the miR-210 function in endothelial cells and study its therapeutic potential in diabetes., Experimental Approach: Two different diabetic mouse models (db/db and Western diet-induced), miR-210 knockout and transgenic mice, isolated vessels and human endothelial cells were used., Key Results: miR-210 levels were lower in aortas isolated from db/db than in control mice. Endothelium-dependent relaxation (EDR) was impaired in aortas from miR-210 knockout mice, and this was restored by inhibiting miR-210 downstream protein tyrosine phosphatase 1B (PTP1B), mitochondrial glycerol-3-phosphate dehydrogenase 2 (GPD2), and mitochondrial oxidative stress. Inhibition of these pathways also improved EDR in both diabetic mouse models. High glucose reduced miR-210 levels in endothelial cells and impaired EDR in mouse aortas, effects that were reversed by overexpressing miR-210. However, plasma miR-210 levels were not affected in individuals with type 2 diabetes (T2D) following improved glycaemic status. Of note, genetic overexpression using miR-210 transgenic mice and pharmacological overexpression using miR-210 mimic in vivo ameliorated endothelial dysfunction in both diabetic mouse models by decreasing PTP1B, GPD2 and oxidative stress. Genetic overexpression of miR-210 altered the aortic transcriptome, decreasing genes in pathways involved in oxidative stress. miR-210 mimic restored decreased nitric oxide production by high glucose in endothelial cells., Conclusion and Implications: This study unravels the mechanisms by which down-regulated miR-210 by high glucose induces endothelial dysfunction in T2D and demonstrates that miR-210 serves as a novel therapeutic target., (© 2024 The Author(s). British Journal of Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society.)

Published
2024
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results