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29 results on '"Bolamperti, Simona"'

8. Ataluren improves myelopoiesis and neutrophil chemotaxis by restoring ribosome biogenesis and reducing p53 levels in Shwachman–Diamond syndrome cells

Author

Cipolli, Marco, primary, Boni, Christian, additional, Penzo, Marianna, additional, Villa, Isabella, additional, Bolamperti, Simona, additional, Baldisseri, Elena, additional, Frattini, Annalisa, additional, Porta, Giovanni, additional, Api, Martina, additional, Selicato, Nora, additional, Roccia, Pamela, additional, Pollutri, Daniela, additional, Marinelli Busilacchi, Elena, additional, Poloni, Antonella, additional, Caporelli, Nicole, additional, D'Amico, Giovanna, additional, Pegoraro, Anna, additional, Cesaro, Simone, additional, Oyarbide, Usua, additional, Vella, Antonio, additional, Lippi, Giuseppe, additional, Corey, Seth J., additional, Valli, Roberto, additional, Polini, Alessandro, additional, and Bezzerri, Valentino, additional

Published
2023
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10. TG-interacting factor 1 (Tgif1)-deficiency attenuates bone remodeling and blunts the anabolic response to parathyroid hormone

Author

Saito, Hiroaki, Gasser, Andreas, Bolamperti, Simona, Maeda, Miki, Matthies, Levi, Jähn, Katharina, Long, Courtney L., Schlüter, Hartmut, Kwiatkowski, Marcel, Saini, Vaibhav, Pajevic, Paola Divieti, Bellido, Teresita, van Wijnen, Andre J., Mohammad, Khalid S., Guise, Theresa A., Taipaleenmäki, Hanna, and Hesse, Eric

Published
2019
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11. Ataluren improves myelopoiesis and neutrophil chemotaxis by restoring ribosome biogenesis and reducing p53 levels in Shwachman–Diamond syndrome cells.

Author

Cipolli, Marco, Boni, Christian, Penzo, Marianna, Villa, Isabella, Bolamperti, Simona, Baldisseri, Elena, Frattini, Annalisa, Porta, Giovanni, Api, Martina, Selicato, Nora, Roccia, Pamela, Pollutri, Daniela, Marinelli Busilacchi, Elena, Poloni, Antonella, Caporelli, Nicole, D'Amico, Giovanna, Pegoraro, Anna, Cesaro, Simone, Oyarbide, Usua, and Vella, Antonio

Subjects
ORGANELLE formation, BONE marrow cells, NEUTROPHILS, NONSENSE mutation, CHEMOTAXIS, EXOCRINE pancreatic insufficiency, RIBOSOMAL proteins
Abstract

Summary: Shwachman–Diamond syndrome (SDS) is characterized by neutropenia, exocrine pancreatic insufficiency and skeletal abnormalities. SDS bone marrow haematopoietic progenitors show increased apoptosis and impairment in granulocytic differentiation. Loss of Shwachman–Bodian–Diamond syndrome (SBDS) expression results in reduced eukaryotic 80S ribosome maturation. Biallelic mutations in the SBDS gene are found in ~90% of SDS patients, ~55% of whom carry the c.183‐184TA>CT nonsense mutation. Several translational readthrough‐inducing drugs aimed at suppressing nonsense mutations have been developed. One of these, ataluren, has received approval in Europe for the treatment of Duchenne muscular dystrophy. We previously showed that ataluren can restore full‐length SBDS protein synthesis in SDS‐derived bone marrow cells. Here, we extend our preclinical study to assess the functional restoration of SBDS capabilities in vitro and ex vivo. Ataluren improved 80S ribosome assembly and total protein synthesis in SDS‐derived cells, restored myelopoiesis in myeloid progenitors, improved neutrophil chemotaxis in vitro and reduced neutrophil dysplastic markers ex vivo. Ataluren also restored full‐length SBDS synthesis in primary osteoblasts, suggesting that its beneficial role may go beyond the myeloid compartment. Altogether, our results strengthened the rationale for a Phase I/II clinical trial of ataluren in SDS patients who harbour the nonsense mutation. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Angiotensin II Modulates Calcium/Phosphate Excretion in Experimental Model of Hypertension: Focus on Bone

Author

Castoldi, Giovanna, primary, Carletti, Raffaella, additional, Ippolito, Silvia, additional, Villa, Isabella, additional, Palmisano, Biagio, additional, Bolamperti, Simona, additional, Rubinacci, Alessandro, additional, Zerbini, Gianpaolo, additional, Meani, Michela, additional, Zatti, Giovanni, additional, and di Gioia, Cira R. T., additional

Published
2022
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14. Angiotensin II Modulates Calcium/Phosphate Excretion in Experimental Model of Hypertension: Focus on Bone

Author

Castoldi, G, Carletti, R, Ippolito, S, Villa, I, Palmisano, B, Bolamperti, S, Rubinacci, A, Zerbini, G, Meani, M, Zatti, G, di Gioia, C, Castoldi, Giovanna, Carletti, Raffaella, Ippolito, Silvia, Villa, Isabella, Palmisano, Biagio, Bolamperti, Simona, Rubinacci, Alessandro, Zerbini, Gianpaolo, Meani, Michela, Zatti, Giovanni, di Gioia, Cira R. T., Castoldi, G, Carletti, R, Ippolito, S, Villa, I, Palmisano, B, Bolamperti, S, Rubinacci, A, Zerbini, G, Meani, M, Zatti, G, di Gioia, C, Castoldi, Giovanna, Carletti, Raffaella, Ippolito, Silvia, Villa, Isabella, Palmisano, Biagio, Bolamperti, Simona, Rubinacci, Alessandro, Zerbini, Gianpaolo, Meani, Michela, Zatti, Giovanni, and di Gioia, Cira R. T.

Abstract

A link between hypertension and long-term bone health has been suggested. The aim of this study was to investigate the effects of chronic angiotensin II administration on urinary calcium/phosphate excretion, bone mineral density, bone remodeling and osteoblast population in a well-established experimental model of hypertension, in the absence of possible confounding factors that could affect bone metabolism. Male Sprague–Dawley rats, divided in the following groups: (a) Angiotensin II (Ang II, 200 ng/kg/min, osmotic minipumps, sub cutis, n = 8); (b) Ang II+losartan (Los, 50 mg/kg/day, per os, n = 6); (c) control group (physiological saline, sub cutis, n = 9); and (d) control+losartan (n = 6) were treated for four weeks. During the experimental period, 24-hour diuresis, urinary calcium, phosphate and sodium excretion were measured prior to the treatment, at two weeks of treatment, and at the end of the treatment. Systolic blood pressure was measured by plethysmography technique (tail cuff method). At the end of the experimental protocol, the rats were euthanized and peripheral quantitative computed tomography at the proximal metaphysis and at the diaphysis of the tibiae and quantitative bone histomorphometry on distal femora were performed. Angiotensin II-dependent hypertension is associated with increased calcium and phosphate excretion. AT1 receptor blockade prevented the increase of blood pressure and phosphate excretion but did not affect the increase of calcium excretion. These changes took place without significantly affecting bone density, bone histology or osteoblast population. In conclusion, in our experimental conditions, angiotensin II-dependent hypertension gave rise to an increased urinary excretion of calcium and phosphate without affecting bone density.

Published
2022

15. Inhibition of FGF23 is a therapeutic strategy to target hematopoietic stem cell niche defects in β-thalassemia.

Author

Aprile, Annamaria, Raggi, Laura, Bolamperti, Simona, Villa, Isabella, Storto, Mariangela, Morello, Gaia, Marktel, Sarah, Tripodo, Claudio, Cappellini, Maria Domenica, Motta, Irene, Rubinacci, Alessandro, and Ferrari, Giuliana

Subjects
HEMATOPOIETIC stem cells, STEM cell niches, FIBROBLAST growth factors, ERYTHROPOIETIN receptors, FETAL hemoglobin, BONE cells, PEPTIDES, BONE marrow
Abstract

Clinical evidence highlights a relationship between the blood and the bone, but the underlying mechanism linking these two tissues is not fully elucidated. Here, we used β-thalassemia as a model of congenital anemia with bone and bone marrow (BM) niche defects. We demonstrate that fibroblast growth factor 23 (FGF23) is increased in patients and mice with β-thalassemia because erythropoietin induces FGF23 overproduction in bone and BM erythroid cells via ERK1/2 and STAT5 pathways. We show that in vivo inhibition of FGF23 signaling by carboxyl-terminal FGF23 peptide is a safe and efficacious therapeutic strategy to rescue bone mineralization and deposition in mice with β-thalassemia, normalizing the expression of niche factors and restoring hematopoietic stem cell (HSC) function. FGF23 may thus represent a molecular link connecting anemia, bone, and the HSC niche. This study provides a translational approach to targeting bone defects and rescuing HSC niche interactions, with potential clinical relevance for improving HSC transplantation and gene therapy for hematopoietic disorders. Editor's summary: Why β-thalassemia results in bone defects in some patients is unclear. Aprile et al. show that the elevated erythropoietin seen in β-thalassemia results in increased fibroblast growth factor 23 (FGF23) in the bone and bone marrow, which can produce bone defects. A small peptide inhibiting FGF23 both restored the bone marrow hematopoietic stem cell niche and rescued bone defects in a mouse model. This study thus ties the blood and bone together in β-thalassemia and demonstrates an avenue to target their pathological interaction. —Catherine A. Charneski [ABSTRACT FROM AUTHOR]

Published
2023
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16. Enhanced p53 Levels Are Involved in the Reduced Mineralization Capacity of Osteoblasts Derived from Shwachman–Diamond Syndrome Subjects

Author

Frattini, Annalisa, primary, Bolamperti, Simona, additional, Valli, Roberto, additional, Cipolli, Marco, additional, Pinto, Rita Maria, additional, Bergami, Elena, additional, Frau, Maria Rita, additional, Cesaro, Simone, additional, Signo, Michela, additional, Bezzerri, Valentino, additional, Porta, Giovanni, additional, Khan, Abdul Waheed, additional, Rubinacci, Alessandro, additional, and Villa, Isabella, additional

Published
2021
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17. Inhibition of Fibroblast Growth Factor-23 (FGF-23) Rescues Bone and Hematopoietic Stem Cell Niche Defects in Beta-Thalassemia, Uncovering the Missing Link between Hematopoiesis and Bone

Author

Aprile, Annamaria, primary, Raggi, Laura, additional, Bolamperti, Simona, additional, Storto, Mariangela, additional, Villa, Isabella, additional, Morello, Gaia, additional, Marktel, Sarah, additional, Tripodo, Claudio, additional, Motta, Irene, additional, Cappellini, Maria Domenica, additional, Rubinacci, Alessandro, additional, and Ferrari, Giuliana, additional

Published
2021
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19. L-Carnitine Reduces Oxidative Stress and Promotes Cells Differentiation and Bone Matrix Proteins Expression in Human Osteoblast-Like Cells

Author

Terruzzi, Ileana, primary, Montesano, Anna, additional, Senesi, Pamela, additional, Villa, Isabella, additional, Ferraretto, Anita, additional, Bottani, Michela, additional, Vacante, Fernanda, additional, Spinello, Alice, additional, Bolamperti, Simona, additional, Luzi, Livio, additional, and Rubinacci, Alessandro, additional

Published
2019
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21. BET-inhibition by JQ1 promotes proliferation and self-renewal capacity of hematopoietic stem cells

Author

Wroblewski, Mark, primary, Scheller-Wendorff, Marina, additional, Udonta, Florian, additional, Bauer, Raimund, additional, Schlichting, Jara, additional, Zhao, Lin, additional, Ben Batalla, Isabel, additional, Gensch, Victoria, additional, Päsler, Sarina, additional, Wu, Lei, additional, Wanior, Marek, additional, Taipaleenmäki, Hanna, additional, Bolamperti, Simona, additional, Najafova, Zeynab, additional, Pantel, Klaus, additional, Bokemeyer, Carsten, additional, Qi, Jun, additional, Hesse, Eric, additional, Knapp, Stefan, additional, Johnsen, Steven, additional, and Loges, Sonja, additional

Published
2018
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29. The Role of Growth Hormone in Mesenchymal Stem Cell Commitment.

Author

Bolamperti, Simona, Guidobono, Francesca, Rubinacci, Alessandro, and Villa, Isabella

Subjects
*MESENCHYMAL stem cells, *SOMATOTROPIN, *CELL determination, *BODY composition, *PROGENITOR cells, *REGENERATIVE medicine
Abstract

Growth hormone (GH) is best known for its prominent role in promoting prepubertal growth and in regulating body composition and metabolism during adulthood. In recent years, the possible role of GH in the modulation of mesenchymal stem cell (MSC) commitment has gained interest. MSCs, characterized by active self-renewal and differentiation potential, express GH receptors. In MSCs derived from different adult tissues, GH induces an inhibition of adipogenic differentiation and favors MSC differentiation towards osteogenesis. This activity of GH indicates that regulation of body composition by GH has already started in the tissue progenitor cells. These findings have fostered research on possible uses of MSCs treated with GH in those pathologies, where a lack of or delays in bone repair occur. After an overview of GH activities, this review will focus on the research that has characterized GH's effects on MSCs and on preliminary studies on the possible application of GH in bone regenerative medicine. [ABSTRACT FROM AUTHOR]

Published
2019
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