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647 results on '"Bianchi, Nicoletta"'

153. Increase of microRNA-210, Decrease of Raptor Gene Expression and Alteration of Mammalian Target of Rapamycin Regulated Proteins following Mithramycin Treatment of Human Erythroid Cells

Author

Bianchi, Nicoletta, primary, Finotti, Alessia, additional, Ferracin, Manuela, additional, Lampronti, Ilaria, additional, Zuccato, Cristina, additional, Breveglieri, Giulia, additional, Brognara, Eleonora, additional, Fabbri, Enrica, additional, Borgatti, Monica, additional, Negrini, Massimo, additional, and Gambari, Roberto, additional

Published
2015
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155. Generation and Characterization of a Transgenic Mouse Carrying a Functional Humanβ-Globin Gene with the IVSI-6 Thalassemia Mutation

Author

Breveglieri, Giulia, primary, Mancini, Irene, additional, Bianchi, Nicoletta, additional, Lampronti, Ilaria, additional, Salvatori, Francesca, additional, Fabbri, Enrica, additional, Zuccato, Cristina, additional, Cosenza, Lucia C., additional, Montagner, Giulia, additional, Borgatti, Monica, additional, Altruda, Fiorella, additional, Fagoonee, Sharmila, additional, Carandina, Gianni, additional, Rubini, Michele, additional, Aiello, Vincenzo, additional, Breda, Laura, additional, Rivella, Stefano, additional, Gambari, Roberto, additional, and Finotti, Alessia, additional

Published
2015
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159. Peptide nucleic acids targeting β-globin mRNAs selectively inhibit hemoglobin production in murine erythroleukemia cells

Author

MONTAGNER, GIULIA, primary, GEMMO, CHIARA, additional, FABBRI, ENRICA, additional, MANICARDI, ALEX, additional, ACCARDO, IGEA, additional, BIANCHI, NICOLETTA, additional, FINOTTI, ALESSIA, additional, BREVEGLIERI, GIULIA, additional, SALVATORI, FRANCESCA, additional, BORGATTI, MONICA, additional, LAMPRONTI, ILARIA, additional, BRESCIANI, ALBERTO, additional, ALTAMURA, SERGIO, additional, CORRADINI, ROBERTO, additional, and GAMBARI, ROBERTO, additional

Published
2014
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160. Production of β-globin and adult hemoglobin following G418 treatment of erythroid precursor cells from homozygous β°39 thalassemia patients

Author

Salvatori, Francesca, Breveglieri, Giulia, Zuccato, Cristina, Finotti, Alessia, Bianchi, Nicoletta, Borgatti, Monica, Feriotto, Giordana, Destro, Federica, Canella, Alessandro, Brognara, Eleonora, Lampronti, Ilaria, Breda, Laura, Rivella, Stefano, Gambari, Roberto, Department of Biochemistry and Molecular Biology, Università degli Studi di Ferrara (UniFE), Biotechnology Center, Department of Pediatric Hematology-Oncology, and Weill Medical College of Cornell University [New York]

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, hemic and lymphatic diseases, Medicine
Abstract

International audience; In several types of thalassemia (including β039-thalassemia) stop codon mutations lead to premature translation termination and to mRNA destabilization through non-sense mediated decay. Drugs (for instance aminoglycosides) can be designed to suppress premature termination, inducing a ribosomal read-through. These findings have introduced new hopes for the development of a pharmacologic approach to the cure of this disease. However, the effects of aminoglycosides on globin mRNA carrying β-thalassemia stop mutations have not yet been investigated. In the present study we have employed a lentiviral construct containing the β039-thalassemia globin gene under control of the β-globin promoter and a LCR cassette. We demonstrated by FACS analysis the production of β-globin by K562 cell clones expressing the β039-thalassemia globin gene and treated with G418. More importantly, after FACS and HPLC analyses, erythroid precursor cells from β039-thalassemia patients were demonstrated to be able to produce β-globin and adult hemoglobin after treatment with G418. This study strongly suggests that ribosomal read-through should be considered a strategy for developing experimental strategies for treatment of β0-thalassemia caused by stop codon mutations.

Published
2009

169. Effects of rapamycin on accumulation of alpha-, beta- and gamma-globin mRNAs in erythroid precursor cells from beta-thalassaemia patients

Author

Eitan, Fibach, Bianchi, Nicoletta, Borgatti, Monica, Zuccato, Cristina, Finotti, Alessia, Lampronti, Ilaria, Eugenia, Prus, Mischiati, Carlo, and Gambari, Roberto

Subjects
erythroid differentiation, Adult, Erythroid Precursor Cells, Male, Sirolimus, gamma-globin, rapamycin, beta-Thalassemia, Drug Evaluation, Preclinical, sickle cell anaemia, Anemia, Sickle Cell, Middle Aged, Kidney Transplantation, beta-thalassaemia, NO, foetal haemoglobin, Globins, Gene Expression Regulation, Humans, Female, Cells, Cultured, Fetal Hemoglobin, Immunosuppressive Agents
Abstract

We studied the effects of rapamycin on cultures of erythroid progenitors derived from the peripheral blood of 10 beta-thalassaemia patients differing widely with respect to their potential to produce foetal haemoglobin (HbF). For this, we employed the two-phase liquid culture procedure for growing erythroid progenitors, high performance liquid chromatography for analysis of HbF production and reverse transcription polymerase chain reaction for quantification of the accumulation of globin mRNAs. The results demonstrated that rapamycin induced an increase of HbF in cultures from all the beta-thalassaemia patients studied and an increase of their overall Hb content/cell. The inducing effect of rapamycin was restricted to gamma-globin mRNA accumulation, being only minor for beta-globin and none for alpha-globin mRNAs. The ability of rapamycin to preferentially increase gamma-globin mRNA content and production of HbF in erythroid precursor cells from beta-thalassaemia patients is of great importance as this agent (also known as sirolimus or rapamune) is already in clinical use as an anti-rejection agent following kidney transplantation. These data suggest that rapamycin warrants further evaluation as a potential therapeutic drug in beta-thalassaemia and sickle cell anaemia.

Published
2006

176. An Aγ-globin G->A gene polymorphism associated with β039 thalassemia globin gene and high fetal hemoglobin production.

Author

Breveglieri, Giulia, Bianchi, Nicoletta, Cosenza, Lucia Carmela, Gamberini, Maria Rita, Chiavilli, Francesco, Zuccato, Cristina, Montagner, Giulia, Borgatti, Monica, Lampronti, Ilaria, Finotti, Alessia, and Gambari, Roberto

Subjects
*GENETIC polymorphisms, *THALASSEMIA, *GLOBIN genes, *FETAL hemoglobin, *GENETIC mutation, *ERYTHROCYTE membranes
Abstract

Background: Increase of the expression of γ-globin gene and high production of fetal hemoglobin (HbF) in β-thalassemia patients is widely accepted as associated with a milder or even asymptomatic disease. The search for HbF-associated polymorphisms (such as the XmnI, BCL11A and MYB polymorphisms) has recently gained great attention, in order to stratify β-thalassemia patients with respect to expectancy of the first transfusion, need for annual intake of blood, response to HbF inducers (the most studied of which is hydroxyurea). Methods: Aγ-globin gene sequencing was performed on genomic DNA isolated from a total of 75 β-thalassemia patients, including 31 β039/β039, 33 β039/β+IVSI-110, 9 β+IVSI-110/β+IVSI-110, one β0IVSI-1/β+IVSI-6 and one β039/β+IVSI-6. Results: The results show that the rs368698783 polymorphism is present in β-thalassemia patients in the 5'UTR sequence (+25) of the Aγ-globin gene, known to affect the LYAR (human homologue of mouse Ly-1 antibody reactive clone) binding site 5'-GGTTAT-3'. This Aγ(+25 G->A) polymorphism is associated with the Gγ-globin-XmnI polymorphism and both are linked with the β039-globin gene, but not with the β+IVSI-110-globin gene. In agreement with the expectation that this mutation alters the LYAR binding activity, we found that the Aγ(+25 G->A) and Gγ-globin-XmnI polymorphisms are associated with high HbF in erythroid precursor cells isolated from β039/β039 thalassemia patients. Conclusions: As a potential explanation of our findings, we hypothesize that in β-thalassemia the Gγ-globin-XmnI/Aγ-globin-(G->A) genotype is frequently under genetic linkage with β0-thalassemia mutations, but not with the β+-thalassemia mutation here studied (i.e. β+IVSI-110) and that this genetic combination has been selected within the population of β0-thalassemia patients, due to functional association with high HbF. Here we describe the characterization of the rs368698783 (+25 G->A) polymorphism of the Aγ-globin gene associated in β039 thalassemia patients with high HbF in erythroid precursor cells. [ABSTRACT FROM AUTHOR]

Published
2017
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183. Accumulation of gamma-globin mRNA in human erythroid cells treated with angelicin

Author

Lampronti, Ilaria, Bianchi, Nicoletta, Borgatti, Monica, Fibach, E, Prus, E, and Gambari, Roberto

Subjects
Erythrocytes, gamma-globin, Gene Expression, NO, beta-thalassemia, sickle cell anemia, Furocoumarins, angelicin, Humans, Hydroxyurea, RNA, Messenger, erythroid differentiation, fetal hemoglobin, Chromatography, High Pressure Liquid, Fetal Hemoglobin, Erythroid Precursor Cells, Reverse Transcriptase Polymerase Chain Reaction, Cytarabine, Glyceraldehyde-3-Phosphate Dehydrogenases, Cell Differentiation, Plicamycin, Globins, Kinetics, Cisplatin, K562 Cells, Cell Division
Abstract

The aim of the present study was to determine whether angelicin is able to increase the expression of gamma-globin genes in human erythroid cells. Angelicin is structurally related to psoralens, a well-known chemical class of photosensitizers used for their antiproliferative activity in treatment of different skin diseases (i.e., psoriasis and vitiligo). To verify the activity of angelicin, we employed two experimental cell systems, the human leukemic K562 cell line and the two-phase liquid culture of human erythroid progenitors isolated from normal donors. The results of our investigation suggest that angelicin, compared with cytosine arabinoside, mithramycin and cisplatin, is a powerful inducer of erythroid differentiation and gamma-globin mRNA accumulation of human leukemia K562 cells. In addition, when normal human erythroid precursors were cultured in the presence of angelicin, increases of gamma-globin mRNA accumulation and fetal hemoglobin (HbF) production, even higher than those obtained using hydroxyurea, were detected. These results could have practical relevance, as pharmacologically-mediated regulation of the expression of human gamma-globin genes, leading to HbF induction, is considered a potential therapeutic approach in hematological disorders, including beta-thalassemia and sickle cell anemia.

Published
2003

200. Therapeutic Hemoglobin Levels after Gene Transfer in β-Thalassemia Mice and in Hematopoietic Cells of β-Thalassemia and Sickle Cells Disease Patients

Author

Breda, Laura, primary, Casu, Carla, additional, Gardenghi, Sara, additional, Bianchi, Nicoletta, additional, Cartegni, Luca, additional, Narla, Mohandas, additional, Yazdanbakhsh, Karina, additional, Musso, Marco, additional, Manwani, Deepa, additional, Little, Jane, additional, Gardner, Lawrence B., additional, Kleinert, Dorothy A., additional, Prus, Eugenia, additional, Fibach, Eitan, additional, Grady, Robert W., additional, Giardina, Patricia J., additional, Gambari, Roberto, additional, and Rivella, Stefano, additional

Published
2012
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