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183 results on '"Crescioli, C"'

6. Testosterone-mediated activation of androgenic signalling sustains in vitro the transformed and radioresistant phenotype of rhabdomyosarcoma cell lines

Author

Giannattasio, S., Megiorni, F., Di Nisio, V., Del Fattore, A., Fontanella, R., Camero, S., Antinozzi, C., Festuccia, C., Gravina, G. L., Cecconi, S., Dominici, C., Di Luigi, L., Ciccarelli, C., De Cesaris, P., Riccioli, A., Zani, B. M., Lenzi, A., Pestell, R. G., Filippini, A., Crescioli, C., Tombolini, V., and Marampon, F.

Published
2019
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13. Sex and Gender Differences in Ischemic Heart Disease: Endocrine Vascular Disease Approach (EVA) Study Design

Author

Raparelli, V., Proietti, M., Lenzi, A., Basili, S., Tiberti, C., Panimolle, F., Isidori, A., Giannetta, E., Napoleone, L., Novo, M., Quattrino, S., Ceccarelli, S., Anastasiadou, E., Marchese, C., Mangieri, E., Tanzilli, G., Viceconte, N., Barilla, F., Gaudio, C., Ettorre, E., Romiti, G. F., Toriello, F., Ruscio, E., Todisco, T., Sperduti, N., Santangelo, G., Visioli, G., Vano, M., Borgi, M., Antonini, L. M., Robuffo, S., Tucci, C., Savoia, M. V., Rossoni, A., Spugnardi, V., Vernile, A., Santoliquido, M., Santori, V., Tosti, G., Recchia, F., Morricone, F., Scacciavillani, R., Lipari, A., Zito, A., Testa, F., Ricci, G., Vellucci, I., Vincenti, M., Pietropaolo, S., Amoroso, D., Stefanini, L., Talerico, G., Pignatelli, P., Bartimoccia, S., Cangemi, R., Minisola, S., Filetti, S., Nocella, C., Pilote, L., Jiri, T. T., Wali, M. A., Kaur, A., Vestri, A. R., Servello, A., Ferroni, P., Crescioli, C., Antinozzi, C., Pignataro, F. S., Bellini, T., Trentini, A., Carnevale, R., Catalano, C., Carbone, I., Galea, N., Bertazzoni, G., Suppa, M., Rosa, A., Scarpellini, M. G., Coppola, A., Illuminati, G., Mariani, P., Neri, F., Salis, P., Segatori, A., Tellini, L., and Costabile, G.

Subjects
Male, 0301 basic medicine, Time Factors, medicine.medical_treatment, Sex steroid hormones, Methods Paper, Myocardial Ischemia, Pharmaceutical Science, Disease, 030204 cardiovascular system & hematology, Coronary Angiography, Translational Research, Biomedical, Settore MED/11, 0302 clinical medicine, Risk Factors, Clinical outcomes, Sex, Platelet function, Myocardial blush grade, Gender, Coronary microvascular dysfunction, Prospective Studies, Registries, Gonadal Steroid Hormones, coronary microvascular dysfunction, gender, myocardial blush grade, platelet function, sex, sex steroid hormones, Genetics (clinical), Prognosis, medicine.anatomical_structure, Research Design, Cardiology, Molecular Medicine, Female, Cardiology and Cardiovascular Medicine, Blood Platelets, medicine.medical_specialty, medicine.drug_class, NO, 03 medical and health sciences, Coronary circulation, Sex Factors, Coronary Circulation, Internal medicine, Genetics, medicine, Humans, Endocrine system, cardiovascular diseases, Healthcare Disparities, Vascular disease, Correction, Percutaneous coronary intervention, Health Status Disparities, medicine.disease, Androgen, 030104 developmental biology, Observational study, Hormone
Abstract

Improvements in ischemic heart disease (IHD) management have been unbalanced between sexes, with coronary microvascular dysfunction considered the likely underlying reason. The Endocrine Vascular disease Approach (EVA) is an observational study (Clinicaltrial.gov NCT02737982) aiming to assess sex and gender interactions between coronary circulation, sexual hormones, and platelet function. Consecutive patients with IHD undergoing coronary angiography will be recruited: (1) to assess sex and gender differences in angiographic reperfusion indexes; (2) to evaluate the effects of estrogen/androgen on sex-related differences in myocardial ischemia; (3) to investigate the platelet biology differences between men and women with IHD; (4) to verify sex- and gender-driven interplay between response to percutaneous coronary intervention, platelets, sex hormones, and myocardial damage at baseline and its impact on 12-month outcomes. The integration of sex and gender in this translational project on IHD will contribute to the identification of new targets for further innovative clinical interventions.

Published
2018

24. Testosterone-mediated activation of androgenic signalling sustains in vitro the transformed and radioresistant phenotype of rhabdomyosarcoma cell lines

Author

Giannattasio, S., primary, Megiorni, F., additional, Di Nisio, V., additional, Del Fattore, A., additional, Fontanella, R., additional, Camero, S., additional, Antinozzi, C., additional, Festuccia, C., additional, Gravina, G. L., additional, Cecconi, S., additional, Dominici, C., additional, Di Luigi, L., additional, Ciccarelli, C., additional, De Cesaris, P., additional, Riccioli, A., additional, Zani, B. M., additional, Lenzi, A., additional, Pestell, R. G., additional, Filippini, A., additional, Crescioli, C., additional, Tombolini, V., additional, and Marampon, F., additional

Published
2018
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38. Methimazole inhibits CXC chemokine ligand 10 secretion in human thyrocytes

Author

Crescioli, C, primary, Cosmi, L, additional, Borgogni, E, additional, Santarlasci, V, additional, Gelmini, S, additional, Sottili, M, additional, Sarchielli, E, additional, Mazzinghi, B, additional, Francalanci, M, additional, Pezzatini, A, additional, Perigli, G, additional, Vannelli, G B, additional, Annunziato, F, additional, and Serio, M, additional

Published
2007
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39. Inhibition of prostate cell growth by BXL-628, a calcitriol analogue selected for a phase II clinical trial in patients with benign prostate hyperplasia

Author

Crescioli, C, primary, Ferruzzi, P, additional, Caporali, A, additional, Scaltriti, M, additional, Bettuzzi, S, additional, Mancina, R, additional, Gelmini, S, additional, Serio, M, additional, Villari, D, additional, Vannelli, GB, additional, Colli, E, additional, Adorini, L, additional, and Maggi, M, additional

Published
2004
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46. Des (1-3) IGF-I-stimulated growth of human stromal BPH cells is inhibited by a vitamin D3 analogue

Author

Crescioli, C., Villari, D., Forti, G., Ferruzzi, P., Petrone, L., Vannelli, G.B., Adorini, L., Salerno, R., Serio, M., and Maggi, M.

Subjects
*PROSTATE hypertrophy, *GROWTH factors, *VITAMIN D
Abstract

Prostate growth and differentiation is under the control of androgens not only during fetal life and childhood but also in adulthood, and it has been proposed that increased prostatic concentration of androgens, or increased androgen responsiveness, causes benign prostatic hyperplasia (BPH). However, different androgen ablation strategies such as treatment with GnRH agonists and finasteride resulted in a modest decrease of the hyperplastic prostate volume. In the last few years it became evident that both androgen-dependent and androgen-independent growth factors promote prostate enlargement by inducing cell proliferation or reducing apoptosis. Therefore, new therapeutic strategies, aimed at reducing intraprostatic growth factor signaling, are under investigation. In this study, we report further evidence that a non hypercalcemic-analogue of vitamin D3, analogue (V) decreases growth factor-induced human BPH cell proliferation and survival. We found that Des (1-3) insulin-like growth factor [Des (1-3) IGF-I], an IGF-I analogue, which does not bind to IGF-binding proteins, is a potent mitogen for BPH stromal cells via a dual mechanism: stimulation of cell growth and inhibition of apoptosis. Similar results were previously reported for another growth factor for BPH cells, keratinocyte growth factor (KGF). Accordingly, we speculate that both KGF and IGF might be involved in the pathogenesis of BPH. We also found analogue (V) not only inhibits the mitogenic activity of growth factors on BPH cells, but even decreased the basal expression of bcl-2, and induced apoptosis. Therefore, vitamin D3 analogues might be considered for the medical treatment of BPH. [Copyright &y& Elsevier]

Published
2002
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48. Bone endothelial cells as estrogen targets.

Author

Brandi, Maria, Crescioli, Clara, Tanini, Annalisa, Frediani, Uliana, Agnusdei, Donato, Gennari, Carlo, Brandi, M L, Crescioli, C, Tanini, A, Frediani, U, Agnusdei, D, and Gennari, C

Subjects
BONE metabolism, PROTEIN analysis, PROTEIN metabolism, ANIMAL experimentation, BONES, CATTLE, CELL culture, CELL differentiation, CELL division, CELLS, COMPARATIVE studies, ENDOTHELIUM, ESTRADIOL, RESEARCH methodology, MEDICAL cooperation, PARATHYROID hormone, PROTEINS, RATS, RECOMBINANT proteins, RESEARCH, RNA, EVALUATION research, CANCER cell culture
Abstract

In the present study, we investigated the effects of estrogens on bone endothelial cell metabolism and the presence of estrogen binding sites in the same cells. For these studies, we have used a continuous cell line of clonal bovine bone endothelial cells for evidence of a direct response to estrogens in vitro. Receptor analysis to intact viable cells was steroid specific and saturable, with an apparent dissociation constant of 17.2 nM and a Bmax of 3.2 x 10(4) sites/cell. Northern blot analysis revealed a 6.5-kilobase mRNA that hybridized with a cDNA to human estrogen receptor. The 6.5-kilobase size is in close agreement with the reported size of the human estrogen receptor mRNA. In vitro estrogen responses of bone endothelial cells included a stimulation of cell proliferation as well as an inhibition of parathyroid hormone responsiveness. These findings clearly demonstrate the presence of functional estrogen receptors in bone endothelial cells in vitro, suggesting a role of estrogens in bone angiogenesis and in the entire process of bone remodeling. [ABSTRACT FROM AUTHOR]

Published
1993
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49. The DAI prospective study on macrovascular complications in patients with type 2 diabetes. Characteristics of the study population

Author

Avogaro, A., carlo giorda, Maggini, M., Mannucci, E., Raschetti, R., Turco, S., Veluss, M., Da Ca, R., Sarli, E., Crescioli, C., Bellis, A., Iacovino, F., Ianni, L., Mencucci, A., Pezzatini, A., Pierazzuoli, E., Pala, L., Sposato, I., Alegiani, S. S., Grosso, J., Capani, F., Ciccarone, A., Pupillo, M., Luca, F., Alfidi, P., Paciotti, V., Venezia, A., Morea, R., Mazzuca, S., Ferraro, M. A., Anastasio, L., Vetrò, T., Caparelli, A., Puccio, L., Iannuzzi, F., Angozzi, G., Pipicelli, G., Tirinato, D., Calatola, P., Malinconico, V., Frullone, S., Mazzocca, S., Pontieri, A., Lutri, Perrelli, A., Carleo, R., Gatti, A., Bonavita, M., Gobbo, M., Creso, E., Giannettino, R., Federico, P., Ragozzino, Torella, R., Masi, R., Santorelli, Sgambato, S., Petraroli, E., De Chiara, Di Giovanni, G., Simone, G., Pappalardo, L., Marro, A., Lucibelli, L., Marrone, M., Caiazzo, G., Gaeta, I., Corigliano, G., Fiordelisi, F., Cresta, G., Pareschi, P., Manservigi, D., Gaiti, D., Manicardi, V., Bosi, E., Magotti, M. G., Trojani, C., Rastelli, E., Marrino, P., Pierfranceschi, D. G., Caronna, S., Ruggiero, F., Castelvetri, G., Brusa, G., D Antonio, C., Parini, S., Savorgnani, M. N., Cernigoi, A. M., Monte, A., Sancandi, M., Maschio, M., Ariatta, M. C., Pellegrini, M. A., Miniussi, P., Donadon, W., Zanette, G., Chiaramonte, F., Serra, M. A., La Saracina, F., Ghisoni, G., Avogaro, A., Giorda, C., Maggini, M., Mannucci, E., Raschetti, R., Turco, S., Veluss, M., Da Ca, R., Sarli, E., Crescioli, C., De Bellis, A., Iacovino, F., Ianni, L., Mencucci, A., Pezzatini, A., Pierazzuoli, E., Pala, L., Sposato, I., Alegiani, S. S., Grosso, J., Capani, F., Ciccarone, A., Pupillo, M., De Luca, F., Alfidi, P., Paciotti, V., Venezia, A., Morea, R., Mazzuca, S., Ferraro, M. A., Anastasio, L., Vetro, T., Caparelli, A., Puccio, L., Iannuzzi, F., Angozzi, G., Pipicelli, G., Tirinato, D., Calatola, P., Malinconico, V., Frullone, S., Mazzocca, S., Pontieri, A., Lutri, Perrelli, A., Carleo, R., Gatti, A., Bonavita, M., Gobbo, M., Creso, E., Giannettino, R., Federico, P., Ragozzino, Torella, R., Masi, R., Santorelli, Sgambato, S., Petraroli, E., De, Chiara, Di Giovanni, G., De Simone, G., Pappalardo, L., Marro, A., Lucibelli, L., Marrone, M., Caiazzo, G., Gaeta, I., Corigliano, G., Fiordelisi, F., Cresta, G., Pareschi, P., Manservigi, D., Gaiti, D., Manicardi, V., Bosi, E., Magotti, M. G., Trojani, C., Rastelli, E., Marrino, P., Pierfranceschi, D. G., Caronna, S., Ruggiero, F., Castelvetri, G., Brusa, G., D'Antonio, C., Parini, S., De Savorgnani, M. N., Cernigoi, A. M., De Monte, A., Sancandi, M., Maschio, M., Ariatta, M. C., Pellegrini, M. A., Miniussi, P., Donadon, W., Zanette, G., Chiaramonte, F., Serra, M. A., La Saracina, F., and Ghisoni, G.

Subjects
Type 2 diabetes mellitus, Cohort study, Macrovascular complications
Abstract

A large multicenter cohort study, the DAI study, is being performed on patients with type 2 diabetes mellitus who are followed by diabetic care units in Italy, to study the prevalence and incidence of myocardial infarction, ischemic heart disease, coronary artery bypass, coronary angioplasty, cerebral thrombo-embolism, and amputations. The reference population consists of all patients visited at the participating units in the period September-December 1998 or March-June 1999. Patients were randomly chosen so as to create a sample representative of the diabetic population visited at the units. Overall, 201 of the approximately 650 Italian diabetic care units participated in the study and 24 094 patients were included in the study. The paper presents the protocol and the characteristics of the DAI study population.

50. Epigenetic Features of Human Perinatal Stem Cells Redefine Their Stemness Potential

Author

Clara Crescioli, Francesco Alviano, Giulia Gaggi, Annalisa Di Ruscio, Angela Di Baldassarre, Andrea Di Credico, Pascal Izzicupo, Barbara Ghinassi, Giovanni Amabile, Ivana Antonucci, Viviana di Giacomo, Gaggi G., Di Credico A., Izzicupo P., Antonucci I., Crescioli C., Di Giacomo V., Di Ruscio A., Amabile G., Alviano F., Di Baldassarre A., and Ghinassi B.

Subjects
Homeobox protein NANOG, Induced Pluripotent Stem Cells, education, SOX2, Biology, OCT4, amniotic epithelial cell, amniotic fluid stem cell, Article, Epigenesis, Genetic, amniotic fluid stem cells, fetal membrane mesenchymal stromal cell, telomere length, perinatal stem cell, Chromosomes, Human, Humans, Epigenetics, Promoter Regions, Genetic, lcsh:QH301-705.5, perinatal stem cells, DNA methylation, integumentary system, Stem Cells, Mesenchymal stem cell, fungi, Infant, Newborn, Telomere Homeostasis, food and beverages, General Medicine, amniotic epithelial cells, Telomere, Cell biology, MicroRNAs, NANOG, lcsh:Biology (General), Gene Expression Regulation, miRNAs expression, Amniotic epithelial cells, embryonic structures, fetal membrane mesenchymal stromal cells, Stem cell
Abstract

Human perinatal stem cells (SCs) can be isolated from fetal annexes without ethical or safety limitations. They are generally considered multipotent, nevertheless, their biological characteristics are still not fully understood. The aim of this study was to investigate the pluripotency potential of human perinatal SCs as compared to human induced pluripotent stem cells (hiPSCs). Despite the low expression of the pluripotent factors NANOG, OCT4, SOX2, and C-KIT in perinatal SC, we observed minor differences in the promoters DNA-methylation profile of these genes with respect to hiPSCs, we also demonstrated that in perinatal SCs miR-145-5p had an inverse trend in comparison to these stemness markers, suggesting that NANOG, OCT4, and SOX2 were regulated at the post-transcriptional level. The reduced expression of stemness markers was also associated with shorter telomere lengths and shift of the oxidative metabolism between hiPSCs and fetal annex-derived cells. Our findings indicate the differentiation ability of perinatal SCs might not be restricted to the mesenchymal lineage due to an epigenetic barrier, but other regulatory mechanisms such as telomere shortening or metabolic changes might impair their differentiation potential and challenge their clinical application.

Published
2020
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