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3. Donepezil-Loaded Nanocarriers for the Treatment of Alzheimer’s Disease: Superior Efficacy of Extracellular Vesicles Over Polymeric Nanoparticles

Author

Oliveira Silva,Rummenigge, Counil,Hermine, Rabanel,Jean-Michel, Haddad,Mohamed, Zaouter,Charlotte, Ben Khedher,Mohamed Raâfet, Patten,Shunmoogum, Ramassamy,Charles, Oliveira Silva,Rummenigge, Counil,Hermine, Rabanel,Jean-Michel, Haddad,Mohamed, Zaouter,Charlotte, Ben Khedher,Mohamed Raâfet, Patten,Shunmoogum, and Ramassamy,Charles

Abstract

Rummenigge Oliveira Silva,1 Hermine Counil,1 Jean-Michel Rabanel,2 Mohamed Haddad,1 Charlotte Zaouter,1 Mohamed Raâfet Ben Khedher,1,3 Shunmoogum A Patten,1 Charles Ramassamy1 1Centre Armand-Frappier Santé Biotechnologie, Institut National de la Recherche Scientifique, Laval, Québec, Canada; 2Faculté de Pharmacie, Université de Montréal, Montréal, Québec, Canada; 3Higher Institute of Biotechnology of Beja, University of Jendouba, Beja, TunisiaCorrespondence: Charles Ramassamy, INRS, Centre Armand-Frappier Santé Biotechnologie, 531 Boul des Prairies, Laval, QC, H7V 1B7, Canada, Tel +450-687 50 10, Email charles.ramassamy@inrs.caIntroduction: Drug delivery across the blood-brain barrier (BBB) is challenging and therefore severely restricts neurodegenerative diseases therapy such as Alzheimer’s disease (AD). Donepezil (DNZ) is an acetylcholinesterase (AChE) inhibitor largely prescribed to AD patients, but its use is limited due to peripheral adverse events. Nanodelivery strategies with the polymer Poly (lactic acid)-poly(ethylene glycol)-based nanoparticles (NPs-PLA-PEG) and the extracellular vesicles (EVs) were developed with the aim to improve the ability of DNZ to cross the BBB, its brain targeting and efficacy.Methods: EVs were isolated from human plasma and PLA-PEG NPs were synthesized by nanoprecipitation. The toxicity, brain targeting capacity and cholinergic activities of the formulations were evaluated both in vitro and in vivo.Results: EVs and NPs-PLA-PEG were designed to be similar in size and charge, efficiently encapsulated DNZ and allowed sustained drug release. In vitro study showed that both formulations EVs-DNZ and NPs-PLA-PEG-DNZ were highly internalized by the endothelial cells bEnd.3. These cells cultured on the Transwell® model were used to analyze the transcytosis of both formulations after validation of the presence of tight junctions, the transendothelial electrical resistance (TEER) values and the permeability of the Dextran-FITC. I

Published
2024

6. BASHY Dyes Are Highly Efficient Lipid Droplet-Targeting Photosensitizers that Induce Ferroptosis through Lipid Peroxidation

Author

Silva, Maria J. S. A., primary, Zhang, Yiyi, additional, Vinck, Robin, additional, Santos, Fábio M. F., additional, António, João P. M., additional, Gourdon-Grünewaldt, Lisa, additional, Zaouter, Charlotte, additional, Castonguay, Annie, additional, Patten, Shunmoogum A., additional, Cariou, Kevin, additional, Boscá, Francisco, additional, Nájera, Francisco, additional, Arteaga, Jesús F., additional, Gasser, Gilles, additional, Pischel, Uwe, additional, and Gois, Pedro M. P., additional

Published
2023
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7. BASHY Dyes Are Highly Efficient Lipid Droplet-targeting Photosensitizers That Induce Ferroptosis Through Lipid Peroxidation

Author

Silva, Maria, primary, Zhang, Yiyi, additional, Vinck, Robin, additional, Santos, Fábio, additional, António, João, additional, Gourdon-Grünewaldt, Lisa, additional, Zaouter, Charlotte, additional, Castonguay, Annie, additional, Patten, Shunmoogum, additional, Cariou, Kevin, additional, Boscá, Francisco, additional, Nájera, Francisco, additional, Arteaga, Jesús, additional, Gasser, Gilles, additional, Pischel, Uwe, additional, and Gois, Pedro, additional

Published
2023
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9. Deep Tissue Penetration of Bottle-Brush Polymers via Cell Capture Evasion and Fast Diffusion

Author

Rabanel, Jean-Michel, primary, Mirbagheri, Marziye, additional, Olszewski, Mateusz, additional, Xie, Guojun, additional, Le Goas, Marine, additional, Latreille, Pierre-Luc, additional, Counil, Hermine, additional, Hervé, Vincent, additional, Silva, Rummenigge Oliveira, additional, Zaouter, Charlotte, additional, Adibnia, Vahid, additional, Acevedo, Mariana, additional, Servant, Marc J., additional, Martinez, Vincent A., additional, Patten, Shunmoogum A., additional, Matyjaszewski, Krzysztof, additional, Ramassamy, Charles, additional, and Banquy, Xavier, additional

Published
2022
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10. Functional variants of POC5 identified in patients with idiopathic scoliosis

Author

Patten, Shunmoogum A., Margaritte-Jeannin, Patricia, Bernard, Jean-Claude, Alix, Eudeline, Labalme, Audrey, Besson, Alicia, Girard, Simon L., Fendri, Khaled, Fraisse, Nicolas, Biot, Bernard, Poizat, Coline, Campan-Fournier, Amandine, Abelin- Genevois, Kariman, Cunin, Vincent, Zaouter, Charlotte, Liao, Meijiang, Lamy, Raphaelle, Lesca, Gaetan, Menassa, Rita, Marcaillou, Charles, Letexier, Melanie, Sanlaville, Damien, Berard, Jerome, Rouleau, Guy A., Clerget-Darpoux, Francoise, Drapeau, Pierre, Moldovan, Florina, and Edery, Patrick

Subjects
Medical research, Medicine, Experimental, Messenger RNA -- Physiological aspects, Scoliosis -- Research, Health care industry
Abstract

Idiopathic scoliosis (IS) is a spine deformity that affects approximately 3% of the population. The underlying causes of IS are not well understood, although there is clear evidence that there is a genetic component to the disease. Genetic mapping studies suggest high genetic heterogeneity, but no IS disease-causing gene has yet been identified. Here, genetic linkage analyses combined with exome sequencing identified a rare missense variant (p.A446T) in the centriolar protein gene POC5 that cosegregated with the disease in a large family with multiple members affected with IS. Subsequently, the p.A446T variant was found in an additional set of families with IS and in an additional 3 cases of IS. Moreover, POC5 variant p.A455P was present and linked to IS in one family and another rare POC5 variant (p.A429V) was identified in an additional 5 cases of IS. In a zebrafish model, expression of any of the 3 human IS-associated POC5 variant mRNAs resulted in spine deformity, without affecting other skeletal structures. Together, these findings indicate that mutations in the POC5 gene contribute to the occurrence of IS., Introduction Idiopathic scoliosis (IS) is a 3D spinal deformity characterized by lateral curvature of the spine of 10° or more, as measured by Cobb's method, and rotation of the vertebral [...]

Published
2015
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17. Adolescent idiopathic scoliosis associated POC5 mutation impairs cell cycle, cilia length and centrosome protein interactions

Author

Hassan, Amani, Parent, Stefan, Mathieu, Hélène, Zaouter, Charlotte, Molidperee, Sirinart, Bagu, Edward T., Barchi, Soraya, Villemure, Isabelle, Patten, Shunmoogum A., Moldovan, Florina, Hassan, Amani, Parent, Stefan, Mathieu, Hélène, Zaouter, Charlotte, Molidperee, Sirinart, Bagu, Edward T., Barchi, Soraya, Villemure, Isabelle, Patten, Shunmoogum A., and Moldovan, Florina

Abstract

Adolescent Idiopathic Scoliosis (AIS) is a spinal deformity that affects approximately 3 percent of human adolescents. Although the etiology and molecular basis of AIS is unclear, several genes such as POC5 have been identified as possible causes of the condition. In order to understand the role of POC5 in the pathogenesis of AIS, we investigated the subcellular localization of POC5 in cilia of cells over-expressing either the wild type (wt) or an AIS-related POC5 variant POC5A429V. Mutation of POC5 was found to alter its subcellular localization and to induce ciliary retraction. Furthermore, we observed an impaired cell-cycle progression with the accumulation of cells in the S-phase in cells expressing POC5A429V. Using immunoprecipitation coupled to mass spectrometry, we identified specific protein interaction partners of POC5, most of which were components of cilia and cytoskeleton. Several of these interactions were altered upon mutation of POC5. Altogether, our results demonstrate major cellular alterations, disturbances in centrosome protein interactions and cilia retraction in cells expressing an AIS-related POC5 mutation. Our study suggests that defects in centrosomes and cilia may underlie AIS pathogenesis.

Published
2019

20. Coded-aperture broadband light field imaging using digital micromirror devices

Author

Liu, Jingdan, Zaouter, Charlotte, Liu, Xianglei, Patten, Shunmoogum A., and Liang, Jinyang

Abstract

Coded-aperture light field (CALF) imaging can record four-dimensional information of incident light rays with a high angular resolution while retaining a camera’s full pixel count. However, existing systems are limited by either imaging speeds and image contrasts of liquid-crystal spatial light modulators or by severe dispersion to broadband light of digital micromirror devices (DMDs), both of which hinder CALF’s widespread applications. Here, we overcome these limitations by developing dispersion-eliminated (DE) CALF imaging. Using a dual-DMD design to compensate for dispersion in the entire visible spectrum, the DECALF imaging system captures 1280×1024×5×5(x,y,θ,φ) color light field images at 20 Hz. Using static and dynamic three-dimensional (3D) color scenes, we experimentally demonstrate multi-perspective viewing, digital refocusing, and 3D tracking of the DECALF imaging system. We also apply it to the imaging and analyses of escape behaviors of freely moving normal and disease-model zebrafish.

Published
2021

21. Human mesenchymal stromal cell-secreted lactate induces M2-macrophage differentiation by metabolic reprogramming

Author

Selleri, Silvia, primary, Bifsha, Panojot, additional, Civini, Sara, additional, Pacelli, Consiglia, additional, Dieng, Mame Massar, additional, Lemieux, William, additional, Jin, Ping, additional, Bazin, Renée, additional, Patey, Natacha, additional, Marincola, Francesco M., additional, Moldovan, Florina, additional, Zaouter, Charlotte, additional, Trudeau, Louis-Eric, additional, Benabdhalla, Basma, additional, Louis, Isabelle, additional, Beauséjour, Christian, additional, Stroncek, David, additional, Le Deist, Françoise, additional, and Haddad, Elie, additional

Published
2016
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