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31 results on '"De Rossi, Giulia"'

4. A study on the roles and effects of syndecans on endothelial cell biology during angiogenesis

Author

De Rossi, Giulia

Subjects
612.1, angiogenesis, Syndecans
Abstract

Angiogenesis, the formation of new blood vessels from pre-existing ones, is a key process during development, wound healing and the female reproductive cycle. However, it is also a pathological feature of many diseases such as cancer, age-related macular degeneration and chronic inflammatory pathologies. Given the complexity underlying the fine regulation of this process, despite the great number of studies, our understanding of it is not yet exhaustive. Syndecans are heparan sulphate proteoglycans with roles in cell adhesion, migration and growth factor interactions. The aim of this body of work was to investigate the role of these molecules in the regulation of angiogenesis. For this purpose, in the first part of my project, I investigated the effects of the extracellular core proteins of all four syndecans on endothelial cell functions. These studies identified that all four proteins are able to inhibit angiogenesis and strongly suppress endothelial cell migration, invasion and tube formation. On the basis of these discoveries, I focused on the syndecan-2 extracellular core protein and showed that it is shed during inflammation and can interact with the endothelial cell surface tyrosine phosphatase receptor CD148. Upon binding to CD148, the syndecan-2 extracellular core protein reduces the expression of active β1 integrins on endothelial cell surface and inhibits endothelial cell migration. This provides a mechanism through which shed syndecan-2 can regulate angiogenesis. Critically, this is an entirely novel pathway for the reduction of angiogenesis which is independent to the main angiogenic factor VEGF. Lastly, since previous works suggested that the syndecan-4-null mouse may exhibit angiogenic defects, I set out to determine the role of syndecan-4 in angiogenesis. Here, I observed an up-regulation of syndecan-4 on endothelial cells in angiogenic settings both in vitro and in vivo. Furthermore, through analysis of in vivo models of pathological angiogenesis, I observed that syndecan-4 is critical for VEGF-A-mediated angiogenesis. This effect was partially explained by impaired activation of VEGFR2 in syndecan-4-null endothelial cells. This data suggests that syndecan- 4 is the main heparan sulphate proteoglycan to act as VEGFR2 co-receptor during pathological angiogenesis. Collectively, the findings of this research have identified previously unknown roles for syndecans in the regulation of angiogenesis.

Published
2016

5. Daily Light Onset and Plasma Membrane Tethers Regulate Mitochondria Redistribution within the Retinal Pigment Epithelium.

Author

Neto, Matilde V., De Rossi, Giulia, Berkowitz, Bruce A., Seabra, Miguel C., Luthert, Philip J., Futter, Clare E., and Burgoyne, Thomas

Subjects
*VISION, *CELL membranes, *CHOROIDEREMIA, *MITOCHONDRIA, *PHAGOSOMES, *RHODOPSIN
Abstract

The retinal pigment epithelium (RPE) is an essential component of the retina that plays multiple roles required to support visual function. These include light onset- and circadian rhythm-dependent tasks, such as daily phagocytosis of photoreceptor outer segments. Mitochondria provide energy to the highly specialized and energy-dependent RPE. In this study, we examined the positioning of mitochondria and how this is influenced by the onset of light. We identified a population of mitochondria that are tethered to the basal plasma membrane pre- and post-light onset. Following light onset, mitochondria redistributed apically and interacted with melanosomes and phagosomes. In a choroideremia mouse model that has regions of the RPE with disrupted or lost infolding of the plasma membrane, the positionings of only the non-tethered mitochondria were affected. This provides evidence that the tethering of mitochondria to the plasma membrane plays an important role that is maintained under these disease conditions. Our work shows that there are subpopulations of RPE mitochondria based on their positioning after light onset. It is likely they play distinct roles in the RPE that are needed to fulfil the changing cellular demands throughout the day. [ABSTRACT FROM AUTHOR]

Published
2024
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6. Ibrutinib-based therapy reinvigorates CD8+ T cells compared to chemoimmunotherapy: immune monitoring from the E1912 trial

Author

Papazoglou, Despoina, primary, Wang, Xin Victoria, additional, Shanafelt, Tait D., additional, Lesnick, Connie E., additional, Ioannou, Nikolaos, additional, De Rossi, Giulia, additional, Herter, Sylvia, additional, Bacac, Marina, additional, Klein, Christian, additional, Tallman, Martin S., additional, Kay, Neil E., additional, and Ramsay, Alan G., additional

Published
2024
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9. Laser-Scribing Optimization for Sprayed SnO2-Based Perovskite Solar Modules on Flexible Plastic Substrates

Author

Babak Taheri, Francesca De Rossi, Giulia Lucarelli, Luigi Angelo Castriotta, Aldo Di Carlo, Thomas M Brown, Francesca Brunetti

Abstract

Flexible perovskite solar cells (FPSCs) are prime candidates for applications requiring a highly efficient, low-cost, lightweight, thin and even foldable power source. Despite record efficiencies of lab-scale flexible devices (19.5% on 0.1 cm2 area), scalability represent a critical factor towards commercialization of FPSCs. Large-area automized deposition techniques and efficient P1-P2-P3 scribing procedures are required to enable high throughput production of flexible perovskite modules (FPSMs), with the latter being much more challenging compared to glass substrates. In this work, we introduce the combined concept of laser scribing optimization and automatized spray-coating of SnO2 layers. Based on a systematic variation of the incident laser power and a comprehensive morphological and electrical analysis of laser-based cell interconnections, optimal scribing parameters are identified. Further, spray-coating is used to deposit uniform compact SnO2 films on large-area (> 120 cm2) plastic substrates. PSCs with spray-coated SnO2 show comparable performance as spin-coated cells, delivering up to 15.3% efficiency on small areas under 1 sun illumination. When upscaling to large areas, FPSMs deliver 12% PCE and negligible hysteresis on 16.8 cm2 and 11.7% PCE on 21.8 cm2 active area, demonstrating that our combined approach is an effective strategy for large-area manufacturing of perovskite devices on flexible substrates.

Published
2022

13. Autophagy modulates endothelial junctions to restrain neutrophil diapedesis during inflammation

Author

Reglero-Real, Natalia, primary, Pérez-Gutiérrez, Lorena, additional, Yoshimura, Azumi, additional, Rolas, Loïc, additional, Garrido-Mesa, José, additional, Barkaway, Anna, additional, Pickworth, Catherine, additional, Saleeb, Rebeca S., additional, Gonzalez-Nuñez, Maria, additional, Austin-Williams, Shani N., additional, Cooper, Dianne, additional, Vázquez-Martínez, Laura, additional, Fu, Tao, additional, De Rossi, Giulia, additional, Golding, Matthew, additional, Voisin, Mathieu-Benoit, additional, Boulanger, Chantal M., additional, Kubota, Yoshiaki, additional, Muller, William A., additional, Tooze, Sharon A., additional, Nightingale, Thomas D., additional, Collinson, Lucy, additional, Perretti, Mauro, additional, Aksoy, Ezra, additional, and Nourshargh, Sussan, additional

Published
2021
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14. CD148 Deficiency in Fibroblasts Promotes the Development of Pulmonary Fibrosis

Author

Tsoyi, Konstantin, primary, Liang, Xiaoliang, additional, De Rossi, Giulia, additional, Ryter, Stefan W., additional, Xiong, Kevin, additional, Chu, Sarah G., additional, Liu, Xiaoli, additional, Ith, Bonna, additional, Celada, Lindsay J., additional, Romero, Freddy, additional, Robertson, Matthew J., additional, Esposito, Anthony J., additional, Poli, Sergio, additional, El-Chemaly, Souheil, additional, Perrella, Mark A., additional, Shi, YuanYuan, additional, Whiteford, James, additional, and Rosas, Ivan O., additional

Published
2021
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16. Pathological Angiogenesis Requires Syndecan-4 for Efficient VEGFA-Induced VE-Cadherin Internalization

Author

De Rossi, Giulia, primary, Vähätupa, Maria, additional, Cristante, Enrico, additional, Arokiasamy, Samantha, additional, Liyanage, Sidath E., additional, May, Ulrike, additional, Pellinen, Laura, additional, Uusitalo-Järvinen, Hannele, additional, Bainbridge, James W., additional, Järvinen, Tero A.H., additional, and Whiteford, James R., additional

Published
2021
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18. Antibody-mediated inhibition of syndecan-4 dimerisation reduces interleukin (IL)-1 receptor trafficking and signalling

Author

Godmann, Lars, primary, Bollmann, Miriam, additional, Korb-Pap, Adelheid, additional, König, Ulrich, additional, Sherwood, Joanna, additional, Beckmann, Denise, additional, Mühlenberg, Katja, additional, Echtermeyer, Frank, additional, Whiteford, James, additional, De Rossi, Giulia, additional, Pap, Thomas, additional, and Bertrand, Jessica, additional

Published
2020
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21. Late neuroprogenitors contribute to normal retinal vascular development in a Hif2a-dependent manner

Author

Cristante, Enrico, primary, Liyanage, Sidath E., additional, Sampson, Robert D., additional, Kalargyrou, Aikaterini, additional, De Rossi, Giulia, additional, Rizzi, Matteo, additional, Hoke, Justin, additional, Ribeiro, Joana, additional, Maswood, Ryea N., additional, Duran, Yanai, additional, Matsuki, Takaaki, additional, Aghaizu, Nozie, additional, Luhmann, Ulrich F., additional, Smith, Alexander J., additional, Ali, Robin R., additional, and Bainbridge, James W. B., additional

Published
2018
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23. Shed syndecan-2 inhibits angiogenesis

Author

De Rossi, Giulia, primary, Evans, Alun R., additional, Kay, Emma, additional, Woodfin, Abigail, additional, McKay, Tristan R., additional, Nourshargh, Sussan, additional, and Whiteford, James R., additional

Published
2014
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26. Ibrutinib-based therapy reinvigorates CD8+T cells compared to chemoimmunotherapy: immune monitoring from the E1912 trial

Author

Papazoglou, Despoina, Wang, Xin Victoria, Shanafelt, Tait D., Lesnick, Connie E., Ioannou, Nikolaos, De Rossi, Giulia, Herter, Sylvia, Bacac, Marina, Klein, Christian, Tallman, Martin S., Kay, Neil E., and Ramsay, Alan G.

Abstract

•Higher effector T-cell numbers and their rejuvenated cytotoxic function accompanies favorable clinical responses to ibrutinib-rituximab.•Enhanced CD8+T-cell lytic synapse activity during ibrutinib-rituximab therapy can be exploited using the bispecific antibody glofitamab.

Published
2023
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27. Extracellular vesicles released by CD40/IL-4–stimulated CLL cells confer altered functional properties to CD4+T cells

Author

Smallwood, Dawn T., Apollonio, Benedetta, Willimott, Shaun, Lezina, Larissa, Alharthi, Afaf, Ambrose, Ashley R., De Rossi, Giulia, Ramsay, Alan G., and Wagner, Simon D.

Abstract

The complex interplay between cancer cells, stromal cells, and immune cells in the tumor microenvironment (TME) regulates tumorigenesis and provides emerging targets for immunotherapies. Crosstalk between CD4+T cells and proliferating chronic lymphocytic leukemia (CLL) tumor B cells occurs within lymphoid tissue pseudofollicles, and investigating these interactions is essential to understand both disease pathogenesis and the effects of immunotherapy. Tumor-derived extracellular vesicle (EV) shedding is emerging as an important mode of intercellular communication in the TME. In order to characterize tumor EVs released in response to T-cell–derived TME signals, we performed microRNA (miRNA [miR]) profiling of EVs released from CLL cells stimulated with CD40 and interleukin-4 (IL-4). Our results reveal an enrichment of specific cellular miRNAs including miR-363 within EVs derived from CD40/IL-4–stimulated CLL cells compared with parental cell miRNA content and control EVs from unstimulated CLL cells. We demonstrate that autologous patient CD4+T cells internalize CLL-EVs containing miR-363 that targets the immunomodulatory molecule CD69. We further reveal that autologous CD4+T cells that are exposed to EVs from CD40/IL-4–stimulated CLL cells exhibit enhanced migration, immunological synapse signaling, and interactions with tumor cells. Knockdown of miR-363 in CLL cells prior to CD40/IL-4 stimulation prevented the ability of CLL-EVs to induce increased synapse signaling and confer altered functional properties to CD4+T cells. Taken together, these data reveal a novel role for CLL-EVs in modifying T-cell function that highlights unanticipated complexity of intercellular communication that may have implications for bidirectional CD4+T-cell:tumor interactions within the TME.

Published
2016
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28. Translating the matrix.

Author

Whiteford, James R, Arokiasamy, Samantha, and De Rossi, Giulia

Subjects
EXTRACELLULAR matrix, MACROMOLECULES, TISSUES, ANIMALS, EXTRACELLULAR space
Abstract

Linked Articles: This article is part of a themed section on Translating the Matrix. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.1/issuetoc. [ABSTRACT FROM AUTHOR]

Published
2019
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29. Autophagy modulates endothelial junctions to restrain neutrophil diapedesis during inflammation

Author

Reglero-Real, Natalia, Pérez-Gutiérrez, Lorena, Yoshimura, Azumi, Rolas, Loïc, Garrido-Mesa, José, Barkaway, Anna, Pickworth, Catherine, Saleeb, Rebeca S, Gonzalez-Nuñez, Maria, Austin-Williams, Shani N, Cooper, Dianne, Vázquez-Martínez, Laura, Fu, Tao, De Rossi, Giulia, Golding, Matthew, Benoit-Voisin, Mathieu, Boulanger, Chantal M, Kubota, Yoshiaki, Muller, William A, Tooze, Sharon A, Nightingale, Thomas D, Collinson, Lucy, Perretti, Mauro, Aksoy, Ezra, and Nourshargh, Sussan

Subjects
Model organisms, Chemical Biology & High Throughput, Signalling & Oncogenes, Cell Biology, Biochemistry & Proteomics, 3. Good health, Imaging
Abstract

The migration of neutrophils from the blood circulation to sites of infection or injury is a key immune response and requires the breaching of endothelial cells (ECs) that line the inner aspect of blood vessels. Unregulated neutrophil transendothelial cell migration (TEM) is pathogenic, but the molecular basis of its physiological termination remains unknown. Here, we demonstrated that ECs of venules in inflamed tissues exhibited a robust autophagic response that was aligned temporally with the peak of neutrophil trafficking and was strictly localized to EC contacts. Genetic ablation of EC autophagy led to excessive neutrophil TEM and uncontrolled leukocyte migration in murine inflammatory models, while pharmacological induction of autophagy suppressed neutrophil infiltration into tissues. Mechanistically, autophagy regulated the remodeling of EC junctions and expression of key EC adhesion molecules, facilitating their intracellular trafficking and degradation. Collectively, we have identified autophagy as a modulator of EC leukocyte trafficking machinery aimed at terminating physiological inflammation.

30. Extracellular vesicles released by CD40/IL-4–stimulated CLL cells confer altered functional properties to CD4+ T cells.

Author

Smallwood, Dawn T., Apollonio, Benedetta, Willimott, Shaun, Lezina, Larissa, Alharthi, Afaf, Ambrose, Ashley R., De Rossi, Giulia, Ramsay, Alan G., and Wagner, Simon D.

Subjects
*VESICLES (Cytology), *TUMOR microenvironment, *CHRONIC lymphocytic leukemia, *B cells, *T cells
Abstract

The complex interplay between cancer cells, stromal cells, and immune cells in the tumor microenvironment (TME) regulates tumorigenesis and provides emerging targets for immunotherapies. Crosstalk between CD4+ T cells and proliferating chronic lymphocytic leukemia (CLL) tumor B cells occurs within lymphoid tissue pseudofollicles, and investigating these interactions is essential to understand both disease pathogenesis and the effects of immunotherapy. Tumor-derived extracellular vesicle (EV) shedding is emerging as an important mode of intercellular communication in the TME. In order to characterize tumor EVs released in response to T-cell-derived TME signals, we performed microRNA (miRNA [miR]) profiling of EVs released from CLL cells stimulated with CD40 and interleukin-4 (IL-4). Our results reveal an enrichment of specific cellular miRNAs including miR-363 within EVs derived from CD40/IL-4-stimulated CLL cells compared with parental cell miRNA content and control EVs from unstimulated CLL cells. We demonstrate that autologous patient CD4+ T cells internalize CLL-EVs containing miR-363 that targets the immunomodulatory molecule CD69. We further reveal that autologous CD4+ T cells that are exposed to EVs from CD40/IL-4-stimulated CLL cells exhibit enhanced migration, immunological synapse signaling, and interactions with tumor cells. Knockdown of miR-363 in CLL cells prior to CD40/IL-4 stimulation prevented the ability of CLL-EVs to induce increased synapse signaling and confer altered functional properties to CD4+ T cells. Taken together, these data reveal a novel role for CLL-EVs in modifying T-cell function that highlights unanticipated complexity of intercellular communication that may have implications for bidirectional CD4+ T-cell:tumor interactions within the TME. [ABSTRACT FROM AUTHOR]

Published
2016
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31. Shed syndecan-2 inhibits angiogenesis.

Author

De Rossi G, Evans AR, Kay E, Woodfin A, McKay TR, Nourshargh S, and Whiteford JR

Subjects
Animals, Cell Movement genetics, Cell Movement physiology, Cells, Cultured, Endothelial Cells metabolism, Humans, Mice, Mice, SCID, Syndecan-2 genetics, Xenograft Model Antitumor Assays, Neovascularization, Pathologic metabolism, Syndecan-2 metabolism
Abstract

Angiogenesis is essential for the development of a normal vasculature, tissue repair and reproduction, and also has roles in the progression of diseases such as cancer and rheumatoid arthritis. The heparan sulphate proteoglycan syndecan-2 is expressed on mesenchymal cells in the vasculature and, like the other members of its family, can be shed from the cell surface resulting in the release of its extracellular core protein. The purpose of this study was to establish whether shed syndecan-2 affects angiogenesis. We demonstrate that shed syndecan-2 regulates angiogenesis by inhibiting endothelial cell migration in human and rodent models and, as a result, reduces tumour growth. Furthermore, our findings show that these effects are mediated by the protein tyrosine phosphatase receptor CD148 (also known as PTPRJ) and this interaction corresponds with a decrease in active β1 integrin. Collectively, these data demonstrate an unexplored pathway for the regulation of new blood vessel formation and identify syndecan-2 as a therapeutic target in pathologies characterised by angiogenesis., (© 2014. Published by The Company of Biologists Ltd.)

Published
2014
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