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1. Early cognitive decline after bilateral subthalamic deep brain stimulation in Parkinson's disease patients with GBA mutations

Author

Benchetrit, Eve, Delaby, Laure, Berthet, Deborah, Danjou, Fabrice, Vidaihlet, Marie, Krack, Paul, Pelissier, Pierre, Morand, Dominique, Delaigue, Christine, Barun, Nadia, Anheim, Mathieu, Pleuvret, Marie, Destée, Alain, Defebvre, Luc, Moreau, Caroline, Simonin, Clémence, Ryckewaert, Gilles, Kreisler, Alexandre, Mutez, Eugénie, Carrière, Nicolas, Hopes, Lucie, Tard, Céline, Grolez, Guillaume, Dujardin, Kathy, Pecheux, Nathalie, Delliaux, Marie, Rolland, Anne-Sophie, Broussolle, Emmanuel, Laurencin, Chloè, Tison, François, Burbaud, Pierre, Mangone, Graziella, Bekadar, Samir, Cormier-Dequaire, Florence, Tahiri, Khadija, Welaratne, Arlette, Czernecki, Virginie, Pineau, Fanny, Karachi, Carine, Castrioto, Anna, Durif, Frank, Tranchant, Christine, Devos, David, Thobois, Stéphane, Meissner, Wassilios G, Navarro, Maria Soledad, Cornu, Philippe, Lesage, Suzanne, Brice, Alexis, Welter, Marie Laure, and Corvol, Jean-Christophe

Published
2020
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6. The autophagy/lysosome pathway is impaired in SCA7 patients and SCA7 knock-in mice

Author

Alves, Sandro, Cormier-Dequaire, Florence, Marinello, Martina, Marais, Thibaut, Muriel, Marie-Paule, Beaumatin, Florian, Charbonnier-Beaupel, Fanny, Tahiri, Khadija, Seilhean, Danielle, El Hachimi, Khalid, Ruberg, Merle, Stevanin, Giovanni, Barkats, Martine, den Dunnen, Wilfred, Priault, Muriel, Brice, Alexis, Durr, Alexandra, Corvol, Jean-Christophe, and Sittler, Annie

Published
2014
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7. Parkinson's disease polygenic risk score is not associated with impulse control disorders: A longitudinal study

Author

Corvol, Jean-Christophe, Elbaz, Alexis, Vidailhet, Marie, Brice, Alexis, Artaud, Fanny, Bourdain, Frédéric, Brandel, Jean-Philippe, Derkinderen, Pascal, Durif, Franck, Levy, Richard, Pico, Fernando, Rascol, Olivier, Bonnet, Anne-Marie, Bonnet, Cecilia, Brefel-Courbon, Christine, Cormier-Dequaire, Florence, Degos, Bertrand, Debilly, Bérangère, Galitsky, Monique, Grabli, David, Hartmann, Andreas, Klebe, Stephan, Kraemmer, Julia, Lacomblez, Lucette, Leder, Sara, Mangone, Graziella, Mariani, Louise-Laure, Marques, Ana-Raquel, Mesnage, Valérie, Muellner, Julia, Ory-Magne, Fabienne, Planté-Bordeneuve, Violaine, Roze, Emmanuel, Tir, Melissa, You, Hana, Benchetrit, Eve, Socha, Julie, Pineau, Fanny, Vidal, Tiphaine, Pomies, Elsa, Bayet, Virginie, Lesage, Suzanne, Tahiri, Khadija, Bertrand, Hélène, Mallet, Alain, Villeret, Coralie, Mazmanian, Merry, Manseur, Hakima, Hajji, Mostafa, Le Toullec, Benjamin, Brochard, Vanessa, Roy, Monica, Rieu, Isabelle, Bernard, Stéphane, Faurie-Grepon, Antoine, Ihle, J., Artaud, F., Bekadar, S., Mangone, G., Sambin, S., Mariani, LL, Bertrand, H., Rascol, O., Durif, F., Derkinderen, P., Scherzer, C., Elbaz, A., and Corvol, JC

Published
2020
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8. (4)_Appendix_1 – Supplemental material for Aging Cartilage in Wild-Type Mice: An Observational Study

Author

Joulnar Akoum, Tahiri, Khadija, Marie-Thérèse Corvol, Borderie, Didier, Étienne, François, Rannou, François, and Nguyen, Christelle

Subjects
FOS: Clinical medicine, FOS: Biological sciences, 110323 Surgery, 110604 Sports Medicine, FOS: Health sciences, 69999 Biological Sciences not elsewhere classified, 110314 Orthopaedics
Abstract

Supplemental material, (4)_Appendix_1 for Aging Cartilage in Wild-Type Mice: An Observational Study by Joulnar Akoum, Khadija Tahiri, Marie-Th�r�se Corvol, Didier Borderie, Fran�ois �tienne, Fran�ois Rannou and Christelle Nguyen in CARTILAGE

Published
2020
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9. The Val158Met COMT polymorphism is a modifier of the age at onset in Parkinsonʼs disease with a sexual dimorphism

Author

Klebe, Stephan, Golmard, Jean-Louis, Nalls, Michael A, Saad, Mohamad, Singleton, Andrew B, Bras, Jose M, Hardy, John, Simon-Sanchez, Javier, Heutink, Peter, Kuhlenbäumer, Gregor, Charfi, Rim, Klein, Christine, Hagenah, Johann, Gasser, Thomas, Wurster, Isabel, Lesage, Suzanne, Lorenz, Delia, Deuschl, Günther, Durif, Franck, Pollak, Pierre, Damier, Philippe, Tison, François, Durr, Alexandra, Amouyel, Philippe, Lambert, Jean-Charles, Tzourio, Christophe, Maubaret, Cécilia, Charbonnier-Beaupel, Fanny, Tahiri, Khadija, Vidailhet, Marie, Martinez, Maria, Brice, Alexis, Corvol, Jean-Christophe, Agid, Y, Anheim, M, Bonnet, A-M, Borg, M, Brice, A., Broussolle, E, Corvol, J-C, Damier, Ph., Destée, A., Durr, A, Durif, F, Klebe, S, Lohmann, E, Martinez, M, Penet, C, Pollak, P, Krack, P, Rascol, O, Tison, F, Tranchant, C, Vérin, M, Viallet, F, Plagnol, Vincent, Bras, Jose M, Hernandez, Dena G, Sharma, Manu, Sheerin, Una-Marie, Saad, Mohamad, Simón-Sánchez, Javier, Schulte, Claudia, Lesage, Suzanne, Sveinbjörnsdóttir, Sigurlaug, Amouyel, Philippe, Arepalli, Sampath, Band, Gavin, Barker, Roger A, Bellinguez, Céline, Ben-Shlomo, Yoav, Berendse, Henk W, Berg, Daniela, Bhatia, Kailash, de Bie, Rob MA, Biffi, Alessandro, Bloem, Bas, Bochdanovits, Zoltan, Bonin, Michael, Brockmann, Kathrin, Brooks, Janet, Burn, David J, Charlesworth, Gavin, Chen, Honglei, Chinnery, Patrick F, Chong, Sean, Clarke, Carl E, Cookson, Mark R, Cooper, J Mark, Corvol, Jean Christophe, Counsell, Carl, Damier, Philippe, Dartigues, Jean-François, Deloukas, Panos, Dexter, David T, van Dijk, Karin D, Dillman, Allissa, Durif, Frank, Edkins, Sarah, Evans, Jonathan R, Foltynie, Thomas, Freeman, Colin, Gao, Jianjun, Gardner, Michelle, Gibbs, Raphael, Goate, Alison, Gray, Emma, Guerreiro, Rita, Gústafsson, Ómar, Harris, Clare, Hellenthal, Garrett, van Hilten, Jacobus J, Hofman, Albert, Hollenbeck, Albert, Holton, Janice, Hu, Michele, Huang, Xuemei, Huber, Heiko, Hudson, Gavin, Hunt, Sarah E, Huttenlocher, Johanna, Illig, Thomas, Jónsson, Pálmi V, Langford, Cordelia, Lees, Andrew, Lichtner, Peter, Limousin, Patricia, Lopez, Grisel, Lorenz, Delia, McNeill, Alisdair, Moorby, Catriona, Morris, Huw, Morrison, Karen E, Mudanohwo, Ese, OʼSullivan, Sean S, Pearson, Justin, Pearson, Richard, Perlmutter, Joel S, Pétursson, Hjörvar, Pirinen, Matti, Pollak, Pierre, Post, Bart, Potter, Simon, Ravina, Bernard, Revesz, Tamas, Riess, Olaf, Rivadeneira, Fernando, Rizzu, Patrizia, Ryten, Mina, Sawcer, Stephen, Schapira, Anthony, Scheffer, Hans, Shaw, Karen, Shoulson, Ira, Sidransky, Ellen, de Silva, Rohan, Smith, Colin, Spencer, Chris CA, Stefánsson, Hreinn, Steinberg, Stacy, Stockton, Joanna D, Strange, Amy, Su, Zhan, Talbot, Kevin, Tanner, Carlie M, Tashakkori-Ghanbaria, Avazeh, Tison, François, Trabzuni, Daniah, Traynor, Bryan J, Uitterlinden, G, Vandrovcova, Jana, Velseboer, Daan, Vidailhet, Marie, Vukcevic, Damjan, Walker, Robert, van de Warrenburg, Bart, Weale, Michael E, Wickremaratchi, Mirdhu, Williams, Nigel, Williams-Gray, Caroline H, Winder-Rhodes, Sophie, Martinez, Maria, Donnelly, Peter, Hardy, John, Heutink, Peter, Brice, Alexis, Gasser, Thomas, Wood, Nicholas W, and Singleton, Andrew B

Published
2013
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10. Early cognitive decline after bilateral subthalamic deep brain stimulation in Parkinson's disease patients with GBA mutations

Author

Mangone, Graziella, primary, Bekadar, Samir, additional, Cormier-Dequaire, Florence, additional, Tahiri, Khadija, additional, Welaratne, Arlette, additional, Czernecki, Virginie, additional, Pineau, Fanny, additional, Karachi, Carine, additional, Castrioto, Anna, additional, Durif, Frank, additional, Tranchant, Christine, additional, Devos, David, additional, Thobois, Stéphane, additional, Meissner, Wassilios G, additional, Navarro, Maria Soledad, additional, Cornu, Philippe, additional, Lesage, Suzanne, additional, Brice, Alexis, additional, Welter, Marie Laure, additional, Corvol, Jean-Christophe, additional, Benchetrit, Eve, additional, Delaby, Laure, additional, Berthet, Deborah, additional, Danjou, Fabrice, additional, Vidaihlet, Marie, additional, Krack, Paul, additional, Pelissier, Pierre, additional, Morand, Dominique, additional, Delaigue, Christine, additional, Barun, Nadia, additional, Anheim, Mathieu, additional, Pleuvret, Marie, additional, Destée, Alain, additional, Defebvre, Luc, additional, Moreau, Caroline, additional, Simonin, Clémence, additional, Ryckewaert, Gilles, additional, Kreisler, Alexandre, additional, Mutez, Eugénie, additional, Carrière, Nicolas, additional, Hopes, Lucie, additional, Tard, Céline, additional, Grolez, Guillaume, additional, Dujardin, Kathy, additional, Pecheux, Nathalie, additional, Delliaux, Marie, additional, Rolland, Anne-Sophie, additional, Broussolle, Emmanuel, additional, Laurencin, Chloè, additional, Tison, François, additional, and Burbaud, Pierre, additional

Published
2020
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11. Parkinson's disease polygenic risk score is not associated with impulse control disorders: A longitudinal study

Author

Ihle, J., primary, Artaud, F., additional, Bekadar, S., additional, Mangone, G., additional, Sambin, S., additional, Mariani, LL, additional, Bertrand, H., additional, Rascol, O., additional, Durif, F., additional, Derkinderen, P., additional, Scherzer, C., additional, Elbaz, A., additional, Corvol, JC, additional, Corvol, Jean-Christophe, additional, Elbaz, Alexis, additional, Vidailhet, Marie, additional, Brice, Alexis, additional, Artaud, Fanny, additional, Bourdain, Frédéric, additional, Brandel, Jean-Philippe, additional, Derkinderen, Pascal, additional, Durif, Franck, additional, Levy, Richard, additional, Pico, Fernando, additional, Rascol, Olivier, additional, Bonnet, Anne-Marie, additional, Bonnet, Cecilia, additional, Brefel-Courbon, Christine, additional, Cormier-Dequaire, Florence, additional, Degos, Bertrand, additional, Debilly, Bérangère, additional, Galitsky, Monique, additional, Grabli, David, additional, Hartmann, Andreas, additional, Klebe, Stephan, additional, Kraemmer, Julia, additional, Lacomblez, Lucette, additional, Leder, Sara, additional, Mangone, Graziella, additional, Mariani, Louise-Laure, additional, Marques, Ana-Raquel, additional, Mesnage, Valérie, additional, Muellner, Julia, additional, Ory-Magne, Fabienne, additional, Planté-Bordeneuve, Violaine, additional, Roze, Emmanuel, additional, Tir, Melissa, additional, You, Hana, additional, Benchetrit, Eve, additional, Socha, Julie, additional, Pineau, Fanny, additional, Vidal, Tiphaine, additional, Pomies, Elsa, additional, Bayet, Virginie, additional, Lesage, Suzanne, additional, Tahiri, Khadija, additional, Bertrand, Hélène, additional, Mallet, Alain, additional, Villeret, Coralie, additional, Mazmanian, Merry, additional, Manseur, Hakima, additional, Hajji, Mostafa, additional, Le Toullec, Benjamin, additional, Brochard, Vanessa, additional, Roy, Monica, additional, Rieu, Isabelle, additional, Bernard, Stéphane, additional, and Faurie-Grepon, Antoine, additional

Published
2020
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17. Oestrogens inhibit interleukin 1(beta)-mediated nitric oxide synthase expression in articular chondrocytes through nuclear factor-(kappa)B impairment

Author

Richette, Pascal, Dumontier, Marie-France, Tahiri, Khadija, Widerak, Magdalena, Torre, Antoine, Benallaloua, Mourad, Rannou, Francois, Corvol, Marie-Therese, and Savouret, Jean-Francois

Subjects
Interleukin-1 -- Research, Nitric oxide -- Research, Gene expression -- Research, Cartilage cells -- Research, Estrogen -- Receptors, Estrogen -- Physiological aspects, Estrogen -- Research, Health
Published
2007

19. Aging Cartilage in Wild-Type Mice: An Observational Study

Author

Akoum, Joulnar, Tahiri, Khadija, Corvol, Marie-Thérèse, Borderie, Didier, Étienne, François, Rannou, François, and Nguyen, Christelle

Abstract

Objective To describe the spontaneous evolution of age-related changes affecting knee joint articular cartilage, walking speed and a serum biomarker of cartilage remodeling in C57BL/6-JRj wild-type male mice.Design Histological changes were assessed by the Osteoarthritis Research Society International (OARSI) score (0=normal, 6=vertical clefts/erosion to the calcified cartilage extending >75% of the articular surface) in newborn, 1-week- and 1-, 3-, 6-, 9- and 12-month-old C57BL/6-JRj wild-type male mice, walking speed by the Locotronic system, and serum C-terminal telopeptide of type II collagen (CTX-II) content by ELISA in 1-, 3-, 6-, and 9-month-old C57BL/6-JRj wild-type male mice.Results Mean (SD) OARSI score significantly increased from 0.2 (0.3) to 1.3 (0.6) (p=0.03) between 1 and 3 months of age and from 1.3 (0.6) to 3.3 (0.6) (p=0.04) between 3 and 6 months of age. Mean walking speed was stable between 1 and 6 months of age but significantly decreased from 11.4 (1.8) to 3.2 (0.8) cm.s-1 (p=0.03) between 6 and 9 months of age. Serum CTX-II content was maximal at 1 month of age, then decreased from 12.2 (8.5) to 2.4 (8.4) pg/ml (p=0.02) between 1 and 3 months of age, remaining low and stable thereafter.Conclusions C57BL/6-JRj wild-type male mice showed continuously increasing osteoarthritic changes but delayed decreasing walking speed with age. These variations were maximal between 3 and 9 months of age. Maximal serum CTX-II content preceded these changes.

Published
2021
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20. Prediction of cognition in Parkinson's disease with a clinical–genetic score: a longitudinal analysis of nine cohorts

Author

Liu, Ganqiang, Locascio, Joseph J, Winder-Rhodes, Sophie, Vidailhet, Marie, Bonnet, Anne-Marie, Bonnet, Cecilia, Corvol, Jean-Christophe, Elbaz, Alexis, Grabli, David, Hartmann, Andreas, Klebe, Stephan, Lacomblez, Lucette, Mangone, Graziella, Tanner, Caroline M, Bourdain, Frédéric, Brandel, Jean-Philippe, Derkinderen, Pascal, Durif, Franck, Mesnage, Valérie, Pico, Fernando, Rascol, Olivier, Brefel-Courbon, Christine, Ory-Magne, Fabienne, Lang, Anthony E, Forlani, Sylvie, Lesage, Suzanne, Tahiri, Khadija, Albin, Roger, Alcalay, Roy, Ascherio, Alberto, Bowman, Dubois, Chen-Plotkin, Alice, Dawson, Ted, Eberly, Shirley, Dewey, Richard, German, Dwight, Saunders-Pullman, Rachel, Scherzer, Clemens, Vaillancourt, David, Petyuk, Vladislav, West, Andy, Zhang, Jing, Brice, Alexis, Ravina, Bernard, Shoulson, Ira, Cormier-Dequaire, Florence, Heutink, Peter, van Hilten, Jacobus J, Barker, Roger A, Williams-Gray, Caroline H, Marinus, Johan, Scherzer, Clemens R, HBS, CamPaIGN, PICNICS, PROPARK, Boot, Brendon, PSG, DIGPD, PDBP, Hyman, Bradley T, Ivinson, Adrian J, Trisini-Lipsanopoulos, Ana, Franco, Daly, Burke, Kyle, Sudarsky, Lewis R, Liao, Zhixiang, Hayes, Michael T, Umeh, Chizoba C, Sperling, Reisa, Growdon, John H, Schwarzschild, Michael A, Hung, Albert Y, Flaherty, Alice W, Blacker, Deborah, Wills, Anne-Marie, Sohur, U Shivraj, Page, Kara, Mejia, Nicte I, Viswanathan, Anand, Gomperts, Stephen N, Khurana, Vikram, Albers, Mark W, Alora-Palli, Maria, McGinnis, Scott, Sharma, Nutan, Dickerson, Bradford, Frosch, Matthew, Gomez-Isla, Teresa, Greenberg, Steven, Gusella, James, Hedden, Trey, Hedley-Whyte, E Tessa, Koenig, Aaron, Marquis-Sayagues, Marta, Marshall, Gad, Okereke, Olivia, Stemmer-Rachaminov, Anat, Kloppenburg, Jessica, Schlossmacher, Michael G, Selkoe, Dennis J, Yi, Thomas, Li, Haining, Stalberg, Gabriel, Jansen, Iris E, Barker, Roger, Foltynie, Tom, Williams-Gray, Caroline, Robbins, Trevor, Brayne, Carol, Mason, Sarah, Breen, David P, Cummins, Gemma, Evans, Jonathan, Mallet, Alain, Neurology, Amsterdam Neuroscience - Neurodegeneration, and Human genetics

Subjects
0301 basic medicine, Gerontology, Male, medicine.medical_specialty, Population, etiology [Cognitive Dysfunction], 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Dementia, Humans, Cognitive Dysfunction, ddc:610, Longitudinal Studies, Cognitive decline, education, Aged, Proportional Hazards Models, Aged, 80 and over, education.field_of_study, Mini–Mental State Examination, Framingham Risk Score, medicine.diagnostic_test, Proportional hazards model, Hazard ratio, Parkinson Disease, Middle Aged, medicine.disease, Prognosis, diagnosis [Dementia], 030104 developmental biology, diagnosis [Cognitive Dysfunction], Quartile, Disease Progression, Female, Neurology (clinical), etiology [Dementia], complications [Parkinson Disease], Psychology, diagnosis [Parkinson Disease], 030217 neurology & neurosurgery, Algorithms
Abstract

Summary Background Cognitive decline is a debilitating manifestation of disease progression in Parkinson's disease. We aimed to develop a clinical–genetic score to predict global cognitive impairment in patients with the disease. Methods In this longitudinal analysis, we built a prediction algorithm for global cognitive impairment (defined as Mini Mental State Examination [MMSE] ≤25) using data from nine cohorts of patients with Parkinson's disease from North America and Europe assessed between 1986 and 2016. Candidate predictors of cognitive decline were selected through a backward eliminated Cox's proportional hazards analysis using the Akaike's information criterion. These were used to compute the multivariable predictor on the basis of data from six cohorts included in a discovery population. Independent replication was attained in patients from a further three independent longitudinal cohorts. The predictive score was rebuilt and retested in 10 000 training and test sets randomly generated from the entire study population. Findings 3200 patients with Parkinson's disease who were longitudinally assessed with 27 022 study visits between 1986 and 2016 in nine cohorts from North America and Europe were assessed for eligibility. 235 patients with MMSE ≤25 at baseline and 135 whose first study visit occurred more than 12 years from disease onset were excluded. The discovery population comprised 1350 patients (after further exclusion of 334 with missing covariates) from six longitudinal cohorts with 5165 longitudinal visits over 12·8 years (median 2·8, IQR 1·6–4·6). Age at onset, baseline MMSE, years of education, motor exam score, sex, depression, and β-glucocerebrosidase ( GBA ) mutation status were included in the prediction model. The replication population comprised 1132 patients (further excluding 14 patients with missing covariates) from three longitudinal cohorts with 19 127 follow-up visits over 8·6 years (median 6·5, IQR 4·1–7·2). The cognitive risk score predicted cognitive impairment within 10 years of disease onset with an area under the curve (AUC) of more than 0·85 in both the discovery (95% CI 0·82–0·90) and replication (95% CI 0·78–0·91) populations. Patients scoring in the highest quartile for cognitive risk score had an increased hazard for global cognitive impairment compared with those in the lowest quartile (hazard ratio 18·4 [95% CI 9·4–36·1]). Dementia or disabling cognitive impairment was predicted with an AUC of 0·88 (95% CI 0·79–0·94) and a negative predictive value of 0·92 (95% 0·88–0·95) at the predefined cutoff of 0·196. Performance was stable in 10 000 randomly resampled subsets. Interpretation Our predictive algorithm provides a potential test for future cognitive health or impairment in patients with Parkinson's disease. This model could improve trials of cognitive interventions and inform on prognosis. Funding National Institutes of Health, US Department of Defense.

Published
2017

23. Transcriptome Analysis of Peripheral Blood in Chronic Inflammatory Demyelinating Polyradiculoneuropathy Patients Identifies TNFR1 and TLR Pathways in the IVIg Response

Author

Richard, Alexandra, primary, Corvol, Jean-Christophe, additional, Debs, Rabab, additional, Reach, Pauline, additional, Tahiri, Khadija, additional, Carpentier, Wassila, additional, Gueguen, Justine, additional, Guillemot, Vincent, additional, Labeyrie, Céline, additional, Adams, David, additional, Viala, Karine, additional, and Cohen Aubart, Fleur, additional

Published
2016
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24. Gene Expression Analyses Identify Narp Contribution in the Development of l-DOPA-Induced Dyskinesia

Author

Charbonnier-Beaupel, Fanny, primary, Malerbi, Marion, additional, Alcacer, Cristina, additional, Tahiri, Khadija, additional, Carpentier, Wassila, additional, Wang, Chuansong, additional, During, Matthew, additional, Xu, Desheng, additional, Worley, Paul F., additional, Girault, Jean-Antoine, additional, Hervé, Denis, additional, and Corvol, Jean-Christophe, additional

Published
2015
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31. Crucial Role of Visfatin/Pre-B Cell Colony-Enhancing Factor in Matrix Degradation and Prostaglandin E2 Synthesis in Chondrocytes.

Author

Gosset, Marjolaine, Berenbaum, Francis, Salvat, Colette, Sautet, Alain, Pigenet, Audrey, Tahiri, Khadija, and Jacques, Claire

Subjects
HORMONES, OSTEOARTHRITIS, CARTILAGE, PROSTAGLANDINS E, PATHOLOGICAL physiology, ADIPOSE tissues
Abstract

The article focuses on a study which analyzed the contribution of adipose tissue-derived hormone visfatin to the pathophysiology of osteoarthritis (OA). The study examined the role of visfatin in prostaglandin E2 (PGE2) synthesis and matrix degradation using real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and immunoblotting. It concluded that visfatin has a catabolic function in cartilage and may play a role in the pathophysiology of OA.

Published
2008
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32. Cell therapy in cartilage repair: cellular and molecular bases

Author

Corvol, Marie-Th?r?se, Tahiri, Khadija, Montembault, Alexandra, Daumard, Alain, Savouret, Jean-Fran?ois, and Rannou, Fran?ois

Abstract

The destruction of articular cartilage represents the outcome of most inflammatory and degenerative rheumatic diseases and leads to severe disability. Articular cartilage being unable to repair spontaneously, alterations of the joint surface often results in end-stage osteoarthritis, requiring surgical intervention and total joint replacement. This makes damaged tissues repair a major challenge in our aging society. Cartilage harbors only one cell type, the chondrocyte, which synthesizes and secretes specific matrix proteins such as type II collagen and high molecular weight proteoglycans. Matrix proteins are responsible for the conservation of the chondrocyte phenotype and the maintenance of the mechanical functions of cartilage. Development of therapeutic strategies for cartilage repair should thus comprise not only the replacement of lost cartilage cells but also that of extracellular matrix with cartilage-like properties. Different protocols are under investigation. The most commonly employed materials include transplantation of autologous osteochondral tissue. More recently, cell-based therapies using autologous mature chondrocytes or pre-chondrogenic stem cells have drawn particular attention. Tissue-engineering procedures represent the actual trend in cartilage repair. This approach combines biodegradable polymeric three-dimensional matrixes and isolated prechondrogenic stem cells. The cells are seeded within the biocompatible matrix and then implanted into the joint. Numerous non-degradable and degradable polymers, which efficiently ?mimic? the natural surroundings of cartilage cells, are currently under investigation. L'augmentation de l'esp?rance de vie rend tr?s urgente la mise au point de techniques de r?paration des tissus l?s?s. Le cartilage articulaire est r?sistant, ?lastique et dure toute la vie. Il permet les mouvements des articulations et prot?ge l'os sous-jacent contre les agressions m?caniques et traumatiques. Mais lorsqu'il est l?s?, le cartilage ne se r?pare pas spontan?ment. Aucun traitement m?dicamenteux n'?tant efficace ? ce jour, il para?t licite d'agir pr?cocement sur les l?sions traumatiques du cartilage de fa?on ? pr?venir l'arthrose et reculer d'autant l'heure de la chirurgie proth?tique. La th?rapie cellulaire pourrait ?tre une voie de pr?vention de la survenue de l'arthrose. Le cartilage ne contient qu'un seul type cellulaire, le chondrocyte qui synth?tise et s?cr?te une abondante matrice prot?ique. Cette derni?re assure le maintien des fonctions m?caniques du cartilage. Le concept de th?rapie cellulaire consiste ? combler la l?sion cartilagineuse non seulement avec des chondrocytes sains, mais aussi ? reconstituer la structure et les propri?t?s physico-chimiques de la matrice. La greffe de chondrocytes autologues est ? la base de ce concept. Les recherches actuelles portent sur l'utilisation de cellules souches ou prog?nitrices, associ?es ? un biomat?riau "intelligent" permettant le maintien du caract?re chondrog?nique des cellules, l'introduction du greffon dans la l?sion articulaire par des m?thodes peu invasives et l'acquisition de propri?t?s m?caniques proches de celle du cartilage natif.

Published
2008

34. SUMOylation by SUMO2 is implicated in the degradation of misfolded ataxin-7 via RNF4 in SCA7 models

Author

Marinello, Martina, Werner, Andreas, Giannone, Mariagiovanna, Tahiri, Khadija, Alves, Sandro, Tesson, Christelle, den Dunnen, Wilfred, Seeler, Jacob-S., Brice, Alexis, and Sittler, Annie

Abstract

Perturbation of protein homeostasis and aggregation of misfolded proteins is a major cause of many human diseases. A hallmark of the neurodegenerative disease spinocerebellar ataxia type 7 (SCA7) is the intranuclear accumulation of mutant, misfolded ataxin-7 (polyQ-ATXN7). Here, we show that endogenous ATXN7 is modified by SUMO proteins, thus also suggesting a physiological role for this modification under conditions of proteotoxic stress caused by the accumulation of polyQ-ATXN7. Co-immunoprecipitation experiments, immunofluorescence microscopy and proximity ligation assays confirmed the colocalization and interaction of polyQ-ATXN7 with SUMO2 in cells. Moreover, upon inhibition of the proteasome, both endogenous SUMO2/3 and the RNF4 ubiquitin ligase surround large polyQ-ATXN7 intranuclear inclusions. Overexpression of RNF4 and/or SUMO2 significantly decreased levels of polyQ-ATXN7 and, upon proteasomal inhibition, led to a marked increase in the polyubiquitination of polyQ-ATXN7. This provides a mechanism for the clearance of polyQ-ATXN7 from affected cells that involves the recruitment of RNF4 by SUMO2/3-modified polyQ-ATXN7, thus leading to its ubiquitination and proteasomal degradation. In a SCA7 knock-in mouse model, we similarly observed colocalization of SUMO2/3 with polyQ-ATXN7 inclusions in the cerebellum and retina. Furthermore, we detected accumulation of SUMO2/3 high-molecular-mass species in the cerebellum of SCA7 knock-in mice, compared with their wild-type littermates, and changes in SUMO-related transcripts. Immunohistochemical analysis showed the accumulation of SUMO proteins and RNF4 in the cerebellum of SCA7 patients. Taken together, our results show that the SUMO pathway contributes to the clearance of aggregated ATXN7 and suggest that its deregulation might be associated with SCA7 disease progression.

Published
2019
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38. Oestrogens inhibit interleukin 1beta-mediated nitric oxide synthase expression in articular chondrocytes through nuclear factor-kappa B impairment.

Author

Richette P, Dumontier MF, Tahiri K, Widerak M, Torre A, Benallaoua M, Rannou F, Corvol MT, and Savouret JF

Subjects
Animals, Cartilage, Articular drug effects, Cartilage, Articular enzymology, Cartilage, Articular metabolism, Cells, Cultured, Chondrocytes drug effects, Chondrocytes metabolism, Dose-Response Relationship, Drug, Estrogen Receptor alpha metabolism, Female, Interleukin-1beta pharmacology, NF-kappa B metabolism, NF-kappa B physiology, Nitric Oxide biosynthesis, Nitric Oxide Synthase genetics, Promoter Regions, Genetic, Rabbits, Signal Transduction drug effects, Transcriptional Activation drug effects, Translocation, Genetic drug effects, Cartilage, Articular cytology, Chondrocytes enzymology, Estradiol pharmacology, Estrogen Receptor alpha physiology, Interleukin-1beta antagonists & inhibitors, Nitric Oxide Synthase metabolism
Abstract

Objectives: To investigate the presence and functionality of oestrogen receptor alpha (ERalpha) in interleukin (IL)1beta-treated rabbit articular chondrocytes in culture, and to determine the mechanisms of 17beta oestradiol (E2) effects on IL1beta-induced inducible nitric oxide synthase (iNOS) expression., Methods: The presence and functionality of ERalpha were investigated by immunocytochemistry and transient expression of an E2-responsive reporter construct. iNOS expression and production were determined by transient expression of a chimeric iNOS promoter-luciferase construct and protein immunoblotting. Nitric oxide (NO) production was determined by the Griess reaction. DNA-binding activities of nuclear factor-kappaB (NF-kappaB) and activated protein 1 were determined by electrophoretic mobility shift assay (EMSA)-ELISA assays. Nuclear translocation of p65 was studied by immunocytochemistry., Results: ERalpha was identified in the nucleus of chondrocytes. ERalpha efficiently transactivated a transiently expressed E2-responsive construct. On IL1beta treatment, ERalpha partially diffused from its nuclear localisation into the cytoplasm and its transactivation ability was impaired. Nevertheless, E2, tamoxifen and raloxifene efficiently inhibited IL1beta-induced NO production (-34%, -31% and -36%, respectively). E2 decreased IL1beta-induced iNOS protein expression (-40%). Transient expression of an iNOS promoter construct strongly suggested that iNOS expression was inhibited at the transcriptional level, and EMSA-ELISA assays showed that E2 reduced (-60%) the IL1beta-induced p65 DNA-binding capacity. Finally, the p65 nuclear translocation induced by IL1beta was also strongly decreased by E2., Conclusions: Our data support a reciprocal antagonism between oestrogens and IL1beta, ultimately resulting in the decrease of cytokine-dependent NO production through transcriptional inhibition of iNOS expression. This effect was associated with selective inhibition of p65 DNA binding and nuclear translocation.

Published
2007
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39. Activation of the peroxisome proliferator-activated receptor alpha pathway potentiates interleukin-1 receptor antagonist production in cytokine-treated chondrocytes.

Author

François M, Richette P, Tsagris L, Fitting C, Lemay C, Benallaoua M, Tahiri K, and Corvol MT

Subjects
Animals, Cartilage Oligomeric Matrix Protein, Cells, Cultured, Chondrocytes drug effects, Chondrocytes metabolism, Clofibrate pharmacology, Extracellular Matrix Proteins metabolism, Glycoproteins metabolism, Interleukin 1 Receptor Antagonist Protein, Interleukin-1 antagonists & inhibitors, Interleukin-1 physiology, Matrilin Proteins, Rabbits, Chondrocytes immunology, PPAR alpha physiology, Sialoglycoproteins biosynthesis
Abstract

Objective: To determine whether peroxisome proliferator-activated receptor alpha (PPARalpha) agonists protect chondrocytes against the effects of interleukin-1beta (IL-1beta)., Methods: PPARalpha expression and function in cultured rabbit articular chondrocytes were studied by Northern blotting, electrophoretic mobility shift assay, and transient expression of a luciferase reporter construct bearing the human IL-1 receptor antagonist (Il-1Ra) gene promoter. Chondrocytes were incubated in vitro with IL-1beta alone or in combination with CloFibrate (CloF) or other PPAR ligands. Proteoglycans were evaluated by 35S-sulfate incorporation, matrix metalloproteinase (MMP) levels were assessed by zymography and enzyme-linked immunosorbent assay (ELISA), and MMP messenger RNA (mRNA) levels were measured by Northern blotting and real-time reverse transcriptase-polymerase chain reaction. IL-1beta and IL-1Ra soluble contents were measured by ELISA., Results: CloF counteracted IL-1beta-induced 35S-proteoglycan degradation, gelatinolytic activity, and MMP-1, -3, and -13 mRNA expression. CloF also maximized IL-1beta-induced endogenous production of soluble IL-1Ra (sIL-1Ra). This stimulating effect on IL-1Ra gene expression was shown, by transient expression assay, to be transcriptional. Inhibition of sIL-1Ra expression by a specific small interfering RNA suppressed the effect of CloF on IL-1beta-induced MMP expression. The stimulatory effect of CloF was enhanced by cotransfection with wild-type PPARalpha and abolished by a dominant-negative PPARalpha mutant. Fenofibrate and WY-14643 displayed a similar stimulating effect on the IL-1Ra promoter, while rosiglitazone did not. Two PPAR response elements, an NF-kappaB-binding site, and a CCAAT/enhancer binding protein-binding site were identified in the IL-1Ra promoter. All 4 sites were necessary for mediation of the effects of CloF., Conclusion: Our findings support the notion that there is a PPARalpha-dependent mechanism that inhibits IL-1beta function in chondrocytes, which operates via an increase in sIL-1Ra production.

Published
2006
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