Malanagahalli Sowmya, Murera Diane, Martín Cristina, Lin Hazel, Wadier Nadége, Dumortier Hélène, Vázquez Ester, Bianco Alberto
Few Layer Graphene Does Not Affect Cellular Homeostasis of Mouse Macrophages Journal Article
In: Nanomaterials (Basel, Switzerland), vol. 10, no. 2, 2020, ISSN: 2079-4991.
Abstract | Links | BibTeX | Tags: Autophagy, bone marrow derived macrophages, carbon nanomaterials, Dumortier, graphene, I2CT, primary immune cells, Team-Bianco, Team-Dumortier
@article{malanagahalli_few_2020,
title = {Few Layer Graphene Does Not Affect Cellular Homeostasis of Mouse Macrophages},
author = {Sowmya Malanagahalli and Diane Murera and Cristina Martín and Hazel Lin and Nadége Wadier and Hélène Dumortier and Ester Vázquez and Alberto Bianco},
doi = {10.3390/nano10020228},
issn = {2079-4991},
year = {2020},
date = {2020-01-01},
journal = {Nanomaterials (Basel, Switzerland)},
volume = {10},
number = {2},
abstract = {: Graphene-related materials (GRMs) are widely used in various applications due to their unique properties. A growing number of reports describe the impact of different carbon nanomaterials, including graphene oxide (GO), reduced GO (rGO), and carbon nanotubes (CNT), on immune cells, but there is still a very limited number of studies on graphene. In this work, we investigated the biological responses of few layer graphene (FLG) on mouse macrophages (bone marrow derived macrophages, BMDMs), which are part of the first line of defense in innate immunity. In particular, our paper describes our findings of short-term FLG treatment in BMDMs with a focus on observing material internalization and changes in general cell morphology. Subsequent investigation of cytotoxicity parameters showed that increasing doses of FLG did not hamper the viability of cells and did not trigger inflammatory responses. Basal level induced autophagic activity sufficed to maintain the cellular homeostasis of FLG treated cells. Our results shed light on the impact of FLG on primary macrophages and show that FLG does not elicit immunological responses leading to cell death.},
keywords = {Autophagy, bone marrow derived macrophages, carbon nanomaterials, Dumortier, graphene, I2CT, primary immune cells, Team-Bianco, Team-Dumortier},
pubstate = {published},
tppubtype = {article}
}
Murera Diane, Malaganahalli Sowmya, Martín Cristina, Reina Giacomo, Fauny Jean-Daniel, Dumortier Hélène, Vázquez Ester, Bianco Alberto
Few layer graphene does not affect the function and the autophagic activity of primary lymphocytes Journal Article
In: Nanoscale, vol. 11, no. 21, pp. 10493–10503, 2019, ISSN: 2040-3372.
Abstract | Links | BibTeX | Tags: Animals, Autophagy, B-Lymphocytes, Dumortier, Graphite, I2CT, Inbred BALB C, Mice, Nanostructures, T-Lymphocytes, Team-Bianco, Team-Dumortier
@article{murera_few_2019,
title = {Few layer graphene does not affect the function and the autophagic activity of primary lymphocytes},
author = {Diane Murera and Sowmya Malaganahalli and Cristina Martín and Giacomo Reina and Jean-Daniel Fauny and Hélène Dumortier and Ester Vázquez and Alberto Bianco},
doi = {10.1039/c9nr00846b},
issn = {2040-3372},
year = {2019},
date = {2019-01-01},
journal = {Nanoscale},
volume = {11},
number = {21},
pages = {10493--10503},
abstract = {Carbon-based nanomaterials represent a new tool in future medical applications. Thus, focusing on the evaluation of the degree of their safety has been growing in the last years. In this study we were particularly interested in understanding the impact of few layer graphene (FLG) on primary murine lymphocytes. These B and T cells, that are the second, but specialized, line of defense of the immune system, rely on various mechanisms to ensure their efficient function and maintenance. One of these mechanisms is autophagy that can be triggered by various nanomaterials in some types of cells. For these reasons, we were interested in evaluating the way FLG could affect this process in lymphocytes. Our results point out that FLG neither impacts the viability and activation of T and B cells nor their autophagic activity. Using confocal microscopy, we were also able to see that FLG does not appear to cause any membrane damage and does not penetrate inside of these cells. Overall, our data do not show any effect of this material on lymphocyte homeostasis, which is one more argument in favor of the continuation of studies investigating the potential of FLG for therapeutic applications.},
keywords = {Animals, Autophagy, B-Lymphocytes, Dumortier, Graphite, I2CT, Inbred BALB C, Mice, Nanostructures, T-Lymphocytes, Team-Bianco, Team-Dumortier},
pubstate = {published},
tppubtype = {article}
}
Lamiable Olivier, Arnold Johan, da de Faria Isaque Joao Silva, Olmo Roenick Proveti, Bergami Francesco, Meignin Carine, Hoffmann Jules A, Marques Joao Trindade, Imler Jean-Luc
Analysis of the Contribution of Hemocytes and Autophagy to Drosophila Antiviral Immunity Journal Article
In: J. Virol., vol. 90, no. 11, pp. 5415–5426, 2016, ISSN: 0022-538X, 1098-5514.
Links | BibTeX | Tags: antiviral immunity, Autophagy, Hemocytes, hoffmann, imler, M3i, meignin
@article{lamiable_analysis_2016,
title = {Analysis of the Contribution of Hemocytes and Autophagy to Drosophila Antiviral Immunity},
author = {Olivier Lamiable and Johan Arnold and Isaque Joao Silva da de Faria and Roenick Proveti Olmo and Francesco Bergami and Carine Meignin and Jules A Hoffmann and Joao Trindade Marques and Jean-Luc Imler},
url = {http://jvi.asm.org/content/90/11/5415},
doi = {10.1128/JVI.00238-16},
issn = {0022-538X, 1098-5514},
year = {2016},
date = {2016-01-01},
urldate = {2016-06-05},
journal = {J. Virol.},
volume = {90},
number = {11},
pages = {5415--5426},
keywords = {antiviral immunity, Autophagy, Hemocytes, hoffmann, imler, M3i, meignin},
pubstate = {published},
tppubtype = {article}
}
Ogawa Michinaga, Yoshikawa Yuko, Kobayashi Taira, Mimuro Hitomi, Fukumatsu Makoto, Kiga Kotaro, Piao Zhenzi, Ashida Hiroshi, Yoshida Mitsutaka, Kakuta Shigeru, Koyama Tomohiro, Goto Yoshiyuki, Nagatake Takahiro, Nagai Shinya, Kiyono Hiroshi, Kawalec Magdalena, Reichhart Jean-Marc, Sasakawa Chihiro
A Tecpr1-dependent selective autophagy pathway targets bacterial pathogens Journal Article
In: Cell Host Microbe, vol. 9, no. 5, pp. 376–389, 2011, ISSN: 1934-6069.
Abstract | Links | BibTeX | Tags: Animals, Autophagy, Biological, Cells, Cultured, M3i, Membrane Proteins, Mice, Microtubule-Associated Proteins, Models, Phagosomes, Protein Interaction Mapping, reichhart, Shigella, Two-Hybrid System Techniques
@article{ogawa_tecpr1-dependent_2011,
title = {A Tecpr1-dependent selective autophagy pathway targets bacterial pathogens},
author = {Michinaga Ogawa and Yuko Yoshikawa and Taira Kobayashi and Hitomi Mimuro and Makoto Fukumatsu and Kotaro Kiga and Zhenzi Piao and Hiroshi Ashida and Mitsutaka Yoshida and Shigeru Kakuta and Tomohiro Koyama and Yoshiyuki Goto and Takahiro Nagatake and Shinya Nagai and Hiroshi Kiyono and Magdalena Kawalec and Jean-Marc Reichhart and Chihiro Sasakawa},
doi = {10.1016/j.chom.2011.04.010},
issn = {1934-6069},
year = {2011},
date = {2011-05-01},
journal = {Cell Host Microbe},
volume = {9},
number = {5},
pages = {376--389},
abstract = {Selective autophagy of bacterial pathogens represents a host innate immune mechanism. Selective autophagy has been characterized on the basis of distinct cargo receptors but the mechanisms by which different cargo receptors are targeted for autophagic degradation remain unclear. In this study we identified a highly conserved Tectonin domain-containing protein, Tecpr1, as an Atg5 binding partner that colocalized with Atg5 at Shigella-containing phagophores. Tecpr1 activity is necessary for efficient autophagic targeting of bacteria, but has no effect on rapamycin- or starvation-induced canonical autophagy. Tecpr1 interacts with WIPI-2, a yeast Atg18 homolog and PI(3)P-interacting protein required for phagophore formation, and they colocalize to phagophores. Although Tecpr1-deficient mice appear normal, Tecpr1-deficient MEFs were defective for selective autophagy and supported increased intracellular multiplication of Shigella. Further, depolarized mitochondria and misfolded protein aggregates accumulated in the Tecpr1-knockout MEFs. Thus, we identify a Tecpr1-dependent pathway as important in targeting bacterial pathogens for selective autophagy.},
keywords = {Animals, Autophagy, Biological, Cells, Cultured, M3i, Membrane Proteins, Mice, Microtubule-Associated Proteins, Models, Phagosomes, Protein Interaction Mapping, reichhart, Shigella, Two-Hybrid System Techniques},
pubstate = {published},
tppubtype = {article}
}