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28 results on '"Lymperi, Stefania"'

6. The effects of postnatal exposure of endocrine disruptors on testicular function: a systematic review and a meta-analysis

Author

Bliatka, Despoina, Nigdelis, Meletios P., Chatzimeletiou, Katerina, Mastorakos, George, Lymperi, Stefania, and Goulis, Dimitrios G.

Abstract

Background: Despite many epidemiological studies having been conducted, the impact of postnatal exposure of endocrine disruptors (EDs) on testicular function remains a controversial issue. Aim: To systematically review the literature and perform a quantitative synthesis to evaluate the effect of EDs on testicular function. Materials and methods: A comprehensive search was conducted in the MEDLINE, Scopus, and CENTRAL databases. Eligible for the systematic review were observational (cross-sectional and cohort) studies with (i) adult men who had a high probability of postnatal exposure to EDs (“exposed”), (ii) adult men who had a low probability of postnatal exposure to EDs (“non-exposed”), and (iii) an outcome of interest [seminal parameters and reproductive hormone concentrations]. The continuous outcomes in each of the studies were synthesized by the random effects model and expressed as standardized mean difference (SMD) with 95% confidence interval (CI). Results: Thirteen studies, including 959 exposed and 907 non-exposed men, fulfilled the inclusion criteria. Exposure to EDs was associated with decreased LH [SMD − 0.17, 95% CI − 0.33 to − 0.02, 10 studies (616 exposed, 563 non-exposed), I240%, p= 0.09], progressive motility [SMD − 0.45, 95% CI − 0.77 to − 0.13, three studies (133 cases, 153 controls), I238%, p= 0.20], and normal morphology [SMD − 0.50, 95% CI − 0.85 to − 0.14, eight studies (562 cases, 540 controls), I287%, p< 0.01] compared with non-exposure. No difference was observed between the other study groups. Conclusions: Postnatal exposure to EDs is associated with decreased semen quality. Nevertheless, there is no evidence that a disruption of testicular function mediates the deterioration in semen quality.

Published
2024
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7. Inhibiting stromal cell heparan sulfate synthesis improves stem cell mobilization and enables engraftment without cytotoxic conditioning

Author

Saez, Borja, Ferraro, Francesca, Yusuf, Rushdia Z., Cook, Colleen M., Yu, Vionnie W.C., Pardo-Saganta, Ana, Sykes, Stephen M., Palchaudhuri, Rahul, Schajnovitz, Amir, Lotinun, Sutada, Lymperi, Stefania, Mendez-Ferrer, Simon, Toro, Raquel del, Day, Robyn, Vasic, Radovan, Acharya, Sanket S., Baron, Roland, Lin, Charles P., Yamaguchi, Yu, Wagers, Amy J., and Scadden, David T.

Published
2014
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10. Expression of genes that regulate follicle development and maturation during ovarian stimulation in poor responders

Author

Vaitsopoulou, Christine I., primary, Kolibianakis, Efstratios M., additional, Bosdou, Julia K., additional, Neofytou, Eirini, additional, Lymperi, Stefania, additional, Makedos, Anastasios, additional, Savvaidou, Despina, additional, Chatzimeletiou, Katerina, additional, Grimbizis, Grigoris F., additional, Lambropoulos, Alexandros, additional, and Tarlatzis, Basil C., additional

Published
2021
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16. A High-Resolution Proteomic Landscaping of Primary Human Dental Stem Cells: Identification of SHED- and PDLSC-Specific Biomarkers

Author

Taraslia, Vasiliki, primary, Lymperi, Stefania, additional, Pantazopoulou, Vasiliki, additional, Anagnostopoulos, Athanasios, additional, Papassideri, Issidora, additional, Basdra, Efthimia, additional, Bei, Marianna, additional, Kontakiotis, Evangelos, additional, Tsangaris, George, additional, Stravopodis, Dimitrios, additional, and Anastasiadou, Ema, additional

Published
2018
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17. Should we expand the indications for varicocele treatment?

Author

Vakalopoulos, Ioannis, primary, Kampantais, Spyridon, additional, Lymperi, Stefania, additional, Grivas, Nikolaos, additional, Ioannidis, Anastasios, additional, Mykoniatis, Ioannis, additional, Nikolaou, Vassilios, additional, and Dimitriadis, Georgios, additional

Published
2017
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18. The Microanatomy of the Leukemic Stem Cell Niche in Murine Chronic Myelogenous Leukemia

Author

Juwell W. Wu, Joel A. Spencer, Richard A. Van Etten, Cher Zhao, Charles Y. Lin, Lymperi Stefania, Daniela S. Krause, David T. Scadden, Cristina Lo Celso, Melanie Meister, and Francesca Ferraro

Subjects
Endosteum, Immunology, Imatinib, Cell Biology, Hematology, Biology, medicine.disease, Biochemistry, Haematopoiesis, medicine.anatomical_structure, Imatinib mesylate, hemic and lymphatic diseases, medicine, Cancer research, Bone marrow, Stem cell, Progenitor cell, medicine.drug, Chronic myelogenous leukemia
Abstract

Objectives and background: Constituents of the bone marrow microenvironment (BMM) influence the proliferation, differentiation and location of hematopoietic stem and progenitor cells (HSPC). Dependent on their maturation stage, different subsets of HSPC are localized at distinct sites in the BMM. This location depends on HSPC-intrinsic, as well as HSPC-extrinsic factors. The BMM protects leukemic stem cells (LSC) from treatment with tyrosine kinase inhibitors or chemotherapy. We, therefore, investigated the microanantomy of the LSC niche hypothesizing that it may differ from the normal HSPC niche. Methods: We used a combination of confocal and 2-photon intravital microscopy (IVM) of the murine calvarium and well-described retroviral models of BCR-ABL1+chronic myelogenous leukemia (CML) and B-cell acute lymphoblastic leukemia (B-ALL). Results: We show here that BCR-ABL1+Lin–c-Kit+Sca-1+ (LKS) CD150+CD48– (LKS SLAM) cells, which harbor the LSC fraction in the CML model, homed to locations further away from the endosteum than their normal counterparts. Prior in-vitro treatment of BCR-ABL1+ LKS with imatinib mesylate, considered standard of care in CML, reversed this phenotype and the cells were found closer to the endosteum. Native BCR-ABL1, as well as the imatinib-resistant BCR-ABL1 point mutants BCR-ABL1Y253F, BCR-ABL1E255K, BCR-ABL1T315I and BCR-ABL1M351T had similar intrinsic catalytic activity, but the BCR-ABL1Y253F, BCR-ABL1E255K, and BCR-ABL1T315I mutants increased the IL-3-independent proliferative capacity of 32D cells relative to native BCR-ABL1. BCR-ABL1Y253F and BCR-ABL1M351T caused increased transformation of primary BM B-lymphoid progenitors in vitro and led to accelerated induction of B-ALL in mice. In the CML model, BCR-ABL1Y253F and BCR-ABL1T315Iinduced myeloproliferative neoplasia with shortened survival and features of accelerated phase disease compared to native BCR-ABL1, whereas BCR-ABL1T315I LKS cells homed closer to osteoblastic cells than LKS cells expressing native BCR-ABL1. Sequential in vivo tracking of leukemic progenitor growth by IVM showed a similar nadir in the number of cells per leukemic cell ‘nest’ 11 days after irradiation and IV transplantation in recipients of DsRed+BCR-ABL1+ or empty vector control-transduced bone marrow. However, between days 18-25 after transplantation there was a significant increase in the number of cells per leukemic cell ‘nest’ compared to the empty vector control group. Sequential immunohistochemistry and TUNEL assays of leukemic bone sections in imatinib- or vehicle-treated recipient mice with CML showed that initial BCR-ABL1+ growth tends to occur at locations further away from the endosteum, whereas erythroid islands were found closer to the endosteum and trabeculae. Apoptosis in response to imatinib appeared most prominent in the metaphysis. Lastly, we could demonstrate by IVM in the CML model that treatment of mice with a combination of imatinib plus granulocyte colony-stimulating factor led to ‘emptying’ of the LSC niche and superior eradication of BCR-ABL1+ leukemic cells compared to treatment with imatinib alone. Conclusions: In summary, these data suggest that the microanatomy of the LSC niche in CML differs from the normal hematopoietic niche. BCR-ABL1 mutation status may affect the positioning of CML LSC in the microenvironment, and location in the niche may be altered pharmacologically, suggesting that niche location may influence clinical outcome. Disclosures Krause: Glycomimetics. Inc.: Research Funding.

Published
2014

22. Specific bone cells produce DLL4 to generate thymus-seeding progenitors from bone marrow

Author

Yu, Vionnie W.C., primary, Saez, Borja, additional, Cook, Colleen, additional, Lotinun, Sutada, additional, Pardo-Saganta, Ana, additional, Wang, Ying-Hua, additional, Lymperi, Stefania, additional, Ferraro, Francesca, additional, Raaijmakers, Marc H.G.P., additional, Wu, Joy Y., additional, Zhou, Lan, additional, Rajagopal, Jayaraj, additional, Kronenberg, Henry M., additional, Baron, Roland, additional, and Scadden, David T., additional

Published
2015
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24. Hematopoietic Stem/Progenitor Cell Retention in the Bone Marrow Depends On Tissue Specific Heparan Sulfate Proteoglycans

Author

Saez, Borja, primary, Ferraro, Francesca, additional, Yusuf, Rushdia Z., additional, Cook, Colleen M, additional, Sykes, Stephen M., additional, Pardo, Ana, additional, Yu, Vionnie W.C., additional, Lotinun, Sutada, additional, Palchaudhuri, Rahul, additional, Lee, Dongjun, additional, Lymperi, Stefania, additional, Day, Robyn, additional, Vasic, Radovan, additional, Acharya, Sanket S., additional, Baron, Roland, additional, Wagers, Amy J., additional, and Scadden, David T., additional

Published
2012
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25. Diabetes Impairs Hematopoietic Stem Cell Mobilization by Altering Niche Function

Author

Ferraro, Francesca, primary, Lymperi, Stefania, additional, Méndez-Ferrer, Simón, additional, Saez, Borja, additional, Spencer, Joel A., additional, Yeap, Beow Y., additional, Masselli, Elena, additional, Graiani, Gallia, additional, Prezioso, Lucia, additional, Rizzini, Elisa Lodi, additional, Mangoni, Marcellina, additional, Rizzoli, Vittorio, additional, Sykes, Stephen M., additional, Lin, Charles P., additional, Frenette, Paul S., additional, Quaini, Federico, additional, and Scadden, David T., additional

Published
2011
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28. Bone marrow mesenchymal stromal cells non-selectively protect chronic myeloid leukemia cells from imatinib-induced apoptosis via the CXCR4/CXCL12 axis.

Author

Vianello F, Villanova F, Tisato V, Lymperi S, Ho KK, Gomes AR, Marin D, Bonnet D, Apperley J, Lam EW, and Dazzi F

Subjects
Animals, Benzamides, Bone Marrow Cells, Chemokine CXCL12 physiology, Coculture Techniques, Humans, Imatinib Mesylate, Mice, Mice, SCID, Receptors, CXCR4 physiology, Stromal Cells, Tumor Cells, Cultured, Apoptosis drug effects, Drug Resistance, Neoplasm, Leukemia, Myelogenous, Chronic, BCR-ABL Positive pathology, Mesenchymal Stem Cells pathology, Piperazines pharmacology, Pyrimidines pharmacology
Abstract

Background: Residual chronic myeloid leukemia disease following imatinib treatment has been attributed to the presence of quiescent leukemic stem cells intrinsically resistant to imatinib. Mesenchymal stromal cells in the bone marrow may favor the persistence and progression of leukemia by preserving the proliferation and self-renewal capacities of the malignant progenitor cells., Design and Methods: BV173 or primary chronic myeloid leukemia cells were co-cultured with human mesenchymal stromal cells and imatinib-induced cell death was then measured. The roles of pro-and anti-apoptotic proteins and chemokine CXCL12 in this context were evaluated. We also studied the ability of BV173 cells to repopulate NOD/SCID mice following in vitro exposure to imatinib and mesenchymal stromal cells., Results: Whilst imatinib induced dose-dependent apoptosis of BV173 cells and primary chronic myeloid leukemia cells, co-culture with mesenchymal stromal cells protected both types of chronic myeloid leukemia cells. Molecular analysis indicated that mesenchymal stromal cells reduced caspase-3 activation and modulated the expression of the anti-apoptotic protein Bcl-XL. Furthermore, chronic myeloid leukemia cells exposed to imatinib in the presence of mesenchymal stromal cells retained the ability to engraft into NOD/SCID mice. We observed that chronic myeloid leukemia cells and mesenchymal stromal cells express functional levels of CXCR4 and CXCL12, respectively. Finally, the CXCR4 antagonist, AMD3100 restored apoptosis by imatinib and the susceptibility of the SCID leukemia repopulating cells to the tyrosine kinase inhibitor., Conclusions: Human mesenchymal stromal cells mediate protection of chronic myeloid leukemia cells from imatinib-induced apoptosis. Disruption of the CXCL12/CXCR4 axis restores, at least in part, the leukemic cells' sensitivity to imatinib. The combination of anti-CXCR4 antagonists with tyrosine kinase inhibitors may represent a powerful approach to the treatment of chronic myeloid leukemia.

Published
2010
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