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9 results on '"Topi, Majlinda"'

1. Specific targeting of inflammatory osteoclastogenesis by the probiotic yeast S. boulardii CNCM I-745 reduces bone loss in osteoporosis

Author

Madel, Maria-Bernadette, primary, Halper, Julia, primary, Ibáñez, Lidia, additional, Claire, Lozano, additional, Rouleau, Matthieu, additional, Boutin, Antoine, additional, Mahler, Adrien, additional, Pontier-Bres, Rodolphe, additional, Ciucci, Thomas, additional, Topi, Majlinda, additional, Hue, Christophe, additional, Amiaud, Jerome, additional, Iborra, Salvador, additional, Sancho, David, additional, Heymann, Dominique, additional, Garchon, Henri-Jean, additional, Czerucka, Dorota, additional, Apparailly, Florence, additional, Duroux-Richard, Isabelle, additional, Wakkach, Abdelilah, additional, and Blin-Wakkach, Claudine, additional

Published
2023
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2. Author response: Specific targeting of inflammatory osteoclastogenesis by the probiotic yeast S. boulardii CNCM I-745 reduces bone loss in osteoporosis

Author

Madel, Maria-Bernadette, primary, Halper, Julia, primary, Ibáñez, Lidia, additional, Claire, Lozano, additional, Rouleau, Matthieu, additional, Boutin, Antoine, additional, Mahler, Adrien, additional, Pontier-Bres, Rodolphe, additional, Ciucci, Thomas, additional, Topi, Majlinda, additional, Hue, Christophe, additional, Amiaud, Jerome, additional, Iborra, Salvador, additional, Sancho, David, additional, Heymann, Dominique, additional, Garchon, Henri-Jean, additional, Czerucka, Dorota, additional, Apparailly, Florence, additional, Duroux-Richard, Isabelle, additional, Wakkach, Abdelilah, additional, and Blin-Wakkach, Claudine, additional

Published
2023
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3. Specific targeting of inflammatory osteoclastogenesis by the probiotic yeast S. boulardii CNCM I-745 reduces bone loss in osteoporosis

Author

Madel, Maria-Bernadette, primary, Halper, Julia, additional, Ibáñez, Lidia, additional, Lozano, Claire, additional, Rouleau, Matthieu, additional, Boutin, Antoine, additional, Pontier-Bres, Rodolphe, additional, Ciucci, Thomas, additional, Topi, Majlinda, additional, Hue, Christophe, additional, Amiaud, Jérôme, additional, Iborra, Salvador, additional, Sancho, David, additional, Heymann, Dominique, additional, Garchon, Henri-Jean, additional, Czerucka, Dorota, additional, Apparailly, Florence, additional, Duroux-Richard, Isabelle, additional, Wakkach, Abdelilah, additional, and Blin-Wakkach, Claudine, additional

Published
2022
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4. Osteoclasts contribute to early development of chronic inflammation by promoting dysregulated hematopoiesis and myeloid skewing

Author

Madel, Maria-Bernadette, primary, Ibáñez, Lidia, additional, Ciucci, Thomas, additional, Halper, Julia, additional, Topi, Majlinda, additional, Garchon, Henri-Jean, additional, Rouleau, Matthieu, additional, Mueller, Christopher G, additional, Peyrin-Biroulet, Laurent, additional, Moulin, David, additional, Blin-Wakkach, Claudine, additional, and Wakkach, Abdelilah, additional

Published
2020
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5. Protective effect of Saccharomyces boulardii CNCM I-745 on the development of inflammatory osteoclasts and inflammatory bone destruction

Author

Madel, Maria-Bernadette, primary, Ibáñez, Lidia, additional, Ciucci, Thomas, additional, Boutin, Antoine, additional, Pontier-Bres, Rodolphe, additional, Hue, Christophe, additional, Topi, Majlinda, additional, Garchon, Henri-Jean, additional, Rouleau, Matthieu, additional, Czerucka, Dorota, additional, Wakkach, Abdelilah, additional, and Blin-Wakkach, Claudine, additional

Published
2020
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6. Autophagy in osteoblasts is involved in mineralization and bone homeostasis

Author

Nollet, Marie, Santucci-Darmanin, Sabine, Breuil, Véronique, Al-Sahlanee, Rasha, Cros, Chantal, Topi, Majlinda, Momier, David, Samson, Michel, Pagnotta, Sophie, Cailleteau, Laurence, Battaglia, Séverine, Farlay, Delphine, Dacquin, Romain, Barois, Nicolas, Jurdic, Pierre, Boivin, Georges, Heymann, Dominique, Lafont, Frank, Lu, Shi Shou, Dempster, David, Carle, Georges, Pierrefite-Carle, Valérie, Carle, Pierre, Transporteurs et Imagerie, Radiothérapie en Oncologie et Mécanismes biologiques des Altérations du Tissu Osseux (TIRO-MATOs - UMR E4320), Service Hospitalier Frédéric Joliot (SHFJ), Université Paris-Saclay-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-UMR E4320 (TIRO-MATOs), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Côte d'Azur (UCA)-Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Côte d'Azur (UCA), Centre Commun de Microscopie Appliquée (CCMA), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA), UMR E4320 (TIRO-MATOs), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Côte d'Azur (UCA)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Côte d'Azur (UCA)-Service Hospitalier Frédéric Joliot (SHFJ), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), and Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay

Subjects
collagen, HRTEM, high resolution transmission electron microscopy, [SDV]Life Sciences [q-bio], Osteoporosis, bone volume, Osteoclasts, TNFSF11/RANKL, runt-related transcription factor 2, TV, Bone remodeling, Mice, Homeostasis, tumor necrosis factor (ligand) superfamily, mineralization, PBS, ComputingMilieux_MISCELLANEOUS, total volume, Microscopy, Confocal, biology, Osteoblast, BECN1, Beclin 1, tartrate resistant, autophagy-related, Cell biology, ACP5/TRAP, medicine.anatomical_structure, RANKL, osteoclast, osteoblast, Female, ribonucleic acid, secreted phosphoprotein 1, medicine.medical_specialty, autophagy, Basic Research Papers, RUNX2, Green Fluorescent Proteins, acid phosphatase 5, Mice, Transgenic, type I, phosphate-buffered saline, Bone and Bones, Bone resorption, SAED, member 11, Osteoclast, Cell Line, Tumor, Internal medicine, bafilomycin A1, medicine, Animals, BV, OC, selected area electron diffraction, OB, Baf, Bone Resorption, Molecular Biology, bone remodeling, microtubule-associated protein 1 light chain 3, Osteoblasts, RANK Ligand, Autophagy, NF-kappa B p50 Subunit, α 1, X-Ray Microtomography, Cell Biology, MAP1LC3 (LC3), medicine.disease, Rats, Oxidative Stress, Endocrinology, TUBB, tubulin, SPP1/OPN, Col1A, biology.protein, RNA, beta
Abstract

International audience; Bone remodeling is a tightly controlled mechanism in which osteoblasts (OB), the cells responsible for bone formation, osteoclasts (OC), the cells specialized for bone resorption, and osteocytes, the multifunctional mechanosensing cells embedded in the bone matrix, are the main actors. Increased oxidative stress in OB, the cells producing and mineralizing bone matrix, has been associated with osteoporosis development but the role of autophagy in OB has not yet been addressed. This is the goal of the present study. We first show that the autophagic process is induced in OB during mineralization. Then, using knockdown of autophagy-essential genes and OB-specific autophagy-deficient mice, we demonstrate that autophagy deficiency reduces mineralization capacity. Moreover, our data suggest that autophagic vacuoles could be used as vehicles in OB to secrete apatite crystals. In addition, autophagy-deficient OB exhibit increased oxidative stress and secretion of the receptor activator of NFKB1 (TNFSF11/RANKL), favoring generation of OC, the cells specialized in bone resorption. In vivo, we observed a 50% reduction in trabecular bone mass in OB-specific autophagy-deficient mice. Taken together, our results show for the first time that autophagy in OB is involved both in the mineralization process and in bone homeostasis. These findings are of importance for mineralized tissues which extend from corals to vertebrates and uncover new therapeutic targets for calcified tissue-related metabolic pathologies.

Published
2014
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9. Autophagy in osteoblasts is involved in mineralization and bone homeostasis.

Author

Nollet M, Santucci-Darmanin S, Breuil V, Al-Sahlanee R, Cros C, Topi M, Momier D, Samson M, Pagnotta S, Cailleteau L, Battaglia S, Farlay D, Dacquin R, Barois N, Jurdic P, Boivin G, Heymann D, Lafont F, Lu SS, Dempster DW, Carle GF, and Pierrefite-Carle V

Subjects
Animals, Bone Remodeling, Bone Resorption, Cell Line, Tumor, Female, Green Fluorescent Proteins metabolism, Homeostasis, Mice, Mice, Transgenic, Microscopy, Confocal, NF-kappa B p50 Subunit metabolism, Osteoclasts metabolism, Oxidative Stress, RANK Ligand metabolism, Rats, X-Ray Microtomography, Autophagy, Bone and Bones metabolism, Osteoblasts cytology
Abstract

Bone remodeling is a tightly controlled mechanism in which osteoblasts (OB), the cells responsible for bone formation, osteoclasts (OC), the cells specialized for bone resorption, and osteocytes, the multifunctional mechanosensing cells embedded in the bone matrix, are the main actors. Increased oxidative stress in OB, the cells producing and mineralizing bone matrix, has been associated with osteoporosis development but the role of autophagy in OB has not yet been addressed. This is the goal of the present study. We first show that the autophagic process is induced in OB during mineralization. Then, using knockdown of autophagy-essential genes and OB-specific autophagy-deficient mice, we demonstrate that autophagy deficiency reduces mineralization capacity. Moreover, our data suggest that autophagic vacuoles could be used as vehicles in OB to secrete apatite crystals. In addition, autophagy-deficient OB exhibit increased oxidative stress and secretion of the receptor activator of NFKB1 (TNFSF11/RANKL), favoring generation of OC, the cells specialized in bone resorption. In vivo, we observed a 50% reduction in trabecular bone mass in OB-specific autophagy-deficient mice. Taken together, our results show for the first time that autophagy in OB is involved both in the mineralization process and in bone homeostasis. These findings are of importance for mineralized tissues which extend from corals to vertebrates and uncover new therapeutic targets for calcified tissue-related metabolic pathologies.

Published
2014
Full Text
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