3 results on '"Camille H. Bourcier"'
Search Results
2. Extracellular traps formation following cervical spinal cord injury
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Pauline Michel‐Flutot, Camille H. Bourcier, Laila Emam, Adeline Gasser, Simon Glatigny, Stéphane Vinit, and Arnaud Mansart
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General Neuroscience - Abstract
Spinal cord injuries involve a primary injury that can lead to permanent loss of function and a secondary injury associated with pathologic and inflammatory processes. Extracellular traps are extracellular structures expressed by immune cells that are primarily composed of chromatin, granular enzymes and histones. Extracellular traps are known to induce tissue damage when overexpressed, and could be associated in the occurrence of secondary damage. In the present study, we used flow cytometry to demonstrate that at 1-day following a C2 spinal cord lateral hemisection in male Swiss mice, resident microglia form vital microglia extracellular traps, and infiltrating neutrophils form vital neutrophil extracellular traps. We also used immunolabelling to show that microglia near the lesion area are most likely to form these microglia extracellular traps. As expected, infiltrating neutrophils are located at the site of injury, though only some of them engage in post-injury extracellular traps formation. We also observed the formation of microglia and neutrophil extracellular traps in our sham animal models of durotomy, but formation was less frequent than following the C2 hemisection. Our results demonstrate for the first time that microglia form extracellular traps in the spinal cord following injury and durotomy. It remains however to determine the mechanisms and kinetics of neutrophil and microglia extracellular traps formation following spinal cord injury. This information would allow to better mitigate this inflammatory process that may contribute to secondary injury, and to effectively target extracellular traps to improve functional outcomes following spinal cord injury.
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- 2022
3. Effects of Chronic High-Frequency rTMS Protocol on Respiratory Neuroplasticity Following C2 Spinal Cord Hemisection in Rats
- Author
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Pauline Michel-Flutot, Isley Jesus, Valentin Vanhee, Camille H. Bourcier, Laila Emam, Abderrahim Ouguerroudj, Kun-Ze Lee, Lyandysha V. Zholudeva, Michael A. Lane, Arnaud Mansart, Marcel Bonay, Stéphane Vinit, Handicap neuromusculaire : Physiopathologie, Biothérapie et Pharmacologies appliquées (END-ICAP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Institut National de la Santé et de la Recherche Médicale (INSERM), Infection et inflammation (2I), National Sun Yat-Sen University (NSYSU), Gladstone Institutes [San Francisco], Drexel University, National Institutes of Health, NIH, National Institute of Neurological Disorders and Stroke, NINDS: F32 NS119348, R01 NS104291, Lisa Dean Moseley Foundation, Institut National de la Santé et de la Recherche Médicale, Inserm, Fondation de France, Ministry of Science and Technology, Taiwan, MOST: 109-2636-B-110-001, Chancellerie des Universités de Paris, Funding: This research was funded by the Chancellerie des Universités de Paris (Legs Poix) (SV, MB), the Fondation de France (SV), the Fondation Médisite (SV), INSERM (MB, SV, AM), Université de Versailles Saint-Quentin-en-Yvelines (SV, AM), the National Institutes of Health, NINDS, R01 NS104291 (MAL) and F32 NS119348 (LVZ), the Lisa Dean Moseley Foundation (MAL), and Ministry of Science and Technology 109-2636-B-110-001 (KZL). The supporters had no role in study design, data collection, and analysis, decision to publish, or preparation of the manuscript., This research was funded by the Chancellerie des Universit?s de Paris (Legs Poix) (SV, MB), the Fondation de France (SV), the Fondation M?disite (SV), INSERM (MB, SV, AM), Universit? de Versailles Saint-Quentin-en-Yvelines (SV, AM), the National Institutes of Health, NINDS, R01 NS104291 (MAL) and F32 NS119348 (LVZ), the Lisa Dean Moseley Foundation (MAL), and Ministry of Science and Technology 109-2636-B-110-001 (KZL). The supporters had no role in study design, data collection, and analysis, decision to publish, or preparation of the manuscript., This study has benefited from the facilities of CYMAGES and histology (UFR SVS, UVSQ, Université Paris-Saclay, 78180 Montigny-le-Bretonneux, France)., and HAL UVSQ, Équipe
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[SDV.IB] Life Sciences [q-bio]/Bioengineering ,General Immunology and Microbiology ,[SDV.MHEP.PHY] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO] ,neuroplasticity ,diaphragm muscle ,repetitive transcranial magnetic stimulation ,spinal cord injury ,General Biochemistry, Genetics and Molecular Biology ,nervous system ,motoneuron excitability ,[SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO] ,phrenic motor network ,[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] ,[SDV.IB]Life Sciences [q-bio]/Bioengineering ,[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] ,General Agricultural and Biological Sciences - Abstract
International audience; High spinal cord injuries (SCIs) lead to permanent diaphragmatic paralysis. The search for therapeutics to induce functional motor recovery is essential. One promising noninvasive therapeutic tool that could harness plasticity in a spared descending respiratory circuit is repetitive transcranial magnetic stimulation (rTMS). Here, we tested the effect of chronic high-frequency (10 Hz) rTMS above the cortical areas in C2 hemisected rats when applied for 7 days, 1 month, or 2 months. An increase in intact hemidiaphragm electromyogram (EMG) activity and excitability (diaphragm motor evoked potentials) was observed after 1 month of rTMS application. Interestingly, despite no real functional effects of rTMS treatment on the injured hemidiaphragm activity during eupnea, 2 months of rTMS treatment strengthened the existing crossed phrenic pathways, allowing the injured hemidiaphragm to increase its activity during the respiratory challenge (i.e., asphyxia). This effect could be explained by a strengthening of respiratory descending fibers in the ventrolateral funiculi (an increase in GAP-43 positive fibers), sustained by a reduction in inflammation in the C1–C3 spinal cord (reduction in CD68 and Iba1 labeling), and acceleration of intracellular plasticity processes in phrenic motoneurons after chronic rTMS treatment. These results suggest that chronic high-frequency rTMS can ameliorate respiratory dysfunction and elicit neuronal plasticity with a reduction in deleterious post-traumatic inflammatory processes in the cervical spinal cord post-SCI. Thus, this therapeutic tool could be adopted and/or combined with other therapeutic interventions in order to further enhance beneficial outcomes.
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- 2022
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