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16. The translocator protein ligand XBD173 improves clinical symptoms and neuropathological markers in the SJL/J mouse model of multiple sclerosis

Author

Marginedas-Freixa, I., Hattab, C., Bouyer, G., Halle, F., Chene, A., Lefevre, S., Cambot, M., Cueff, A., Schmitt, M., Gamain, B., Lacapere, J., Egee, S., Le Van Kim, C., Ostuni, M., Leva, Géraldine, Klein, Christian, Benyounes, Jérémie, Hallé, François, Bihel, Frédéric, Collongues, Nicolas, De Sèze, Jérôme, Mensah-Nyagan, Ayikoe-Guy, Patte-Mensah, Christine, Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER, Laboratoire Univers et Théories (LUTH (UMR_8102)), Institut national des sciences de l'Univers (INSU - CNRS)-Observatoire de Paris, Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7), Acides Nucléiques : Régulations Naturelle et Artificielle (ARNA), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Chimie du CNRS (INC)-Université de Bordeaux (UB), Laboratoire d'Innovation Thérapeutique (LIT), Université de Strasbourg (UNISTRA)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Service de Neurologie [Strasbourg], CHU Strasbourg-Hopital Civil, Service de neurologie [Strasbourg], CHU Strasbourg, Biopathologie de la Myéline, Neuroprotection et Stratégies Thérapeutiques (BMNST), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut des Neurosciences Cellulaires et Intégratives (INCI), Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique (CNRS), Université de Bordeaux (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Institut de Chimie du CNRS (INC), Centre de Thermique de Lyon (CETHIL), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS), Centre Régional de Lutte contre le cancer - Centre Georges-François Leclerc (CRLCC - CGFL), PSL Research University (PSL)-PSL Research University (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Université de Bordeaux (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), and Biopathologie de la Myéline, Neuroprotection et Stratégies Thérapeutiques

Subjects
0301 basic medicine, Encephalomyelitis, Autoimmune, Experimental, [SDV]Life Sciences [q-bio], Mice, Inbred Strains, Pregnanolone, [CHIM.THER]Chemical Sciences/Medicinal Chemistry, Ligands, Mice, 03 medical and health sciences, Multiple Sclerosis, Relapsing-Remitting, 0302 clinical medicine, Receptors, GABA, immune system diseases, medicine, Translocator protein, Animals, [CHIM]Chemical Sciences, RNA, Messenger, Molecular Biology, Neuroinflammation, ComputingMilieux_MISCELLANEOUS, Autoimmune disease, Neurotransmitter Agents, biology, business.industry, Multiple sclerosis, Experimental autoimmune encephalomyelitis, Neurodegeneration, Brain, Myelin Basic Protein, medicine.disease, nervous system diseases, 3. Good health, Emapunil, Myelin basic protein, 030104 developmental biology, Spinal Cord, Purines, Immunology, biology.protein, Cytokines, Molecular Medicine, Female, business, Biomarkers, 030217 neurology & neurosurgery, Demyelinating Diseases
Abstract

Multiple sclerosis (MS) is a severe autoimmune disease characterized by inflammatory, demyelinating and neurodegenerative components causing motor, sensory, visual and/or cognitive symptoms. The relapsing-remitting MS affecting 85% of patients is reliably mimicked by the proteolipid-protein (PLP)-induced experimental autoimmune encephalomyelitis (EAE) SJL/J-mouse model. Significant progress was made for MS treatment but the development of effective therapies devoid of severe side-effects remains a great challenge. Here, we combine clinical, behavioral, histopathological, biochemical and molecular approaches to demonstrate that low and well tolerated doses (10-20mg/kg) of TSPO ligand XBD173 (Emapunil) efficiently ameliorate clinical signs and neuropathology of PLP-EAE mice. In addition to the conventional clinical scoring of symptoms, we applied the robust behavioral Catwalk-method to confirm that XBD173 (10mg/kg) increases the maximum contact area parameter at EAE-disease peak, indicating an improvement/recovery of motor functions. Consistently, histopathological studies coupled with microscope-cellSens quantification and RT-qPCR analyzes showed that XBD173 prevented demyelination by restoring normal protein and mRNA levels of myelin basic protein that was significantly repressed in PLP-EAE mice spinal cord and brain. Interestingly, ELISA-based measurement revealed that XBD173 increased allopregnanolone concentrations in PLP-EAE mice spinal and brain tissues. Furthermore, flow cytometry assessment demonstrated that XBD173 therapy decreased serum level of pro-inflammatory cytokines, including interleukin-17A, Interleukin-6 and tumor-necrosis-factor alpha in PLP-EAE mice. As the optimal XBD173 dosing exerting the maximal beneficial action in EAE mice is the lower 10mg/kg dose, the paper opens interesting perspectives for the development of efficient and safe therapies against MS with slight or no side-effects.

Published
2017
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17. Rapid Cl-/HCOFormula exchange kinetics of AE1 in HEK293 cells and hereditary stomatocytosis red blood cells

Author

Frumence E, Genetet S, Ripoche P, Le Van Kim C, Colin Y, Mouro Chanteloup I, Lopez C., IOLASCON, ACHILLE, ANDOLFO, IMMACOLATA, Frumence, E, Genetet, S, Ripoche, P, Iolascon, Achille, Andolfo, Immacolata, Le Van Kim, C, Colin, Y, Mouro Chanteloup, I, and Lopez, C.

Abstract

Anion exchanger 1 (AE1) or band 3 is a membrane protein responsible for the rapid exchange of chloride for bicarbonate across the red blood cell membrane. Nine mutations leading to single amino-acid substitutions in the transmembrane domain of AE1 are associated with dominant hereditary stomatocytosis, monovalent cation leaks, and reduced anion exchange activity. We set up a stopped-flow spectrofluorometry assay coupled with flow cytometry to investigate the anion transport and membrane expression characteristics of wild-type recombinant AE1 in HEK293 cells, using an inducible expression system. Likewise, study of three stomatocytosis-associated mutations (R730C, E758K, and G796R), allowed the validation of our method. Measurement of the rapid and specific chloride/bicarbonate exchange by surface expressed AE1 showed that E758K mutant was fully active compared with wild-type (WT) AE1, whereas R730C and G796R mutants were inactive, reinforcing previously reported data on other experimental models. Stopped-flow analysis of AE1 transport activity in red blood cell ghost preparations revealed a 50% reduction of G796R compared with WT AE1 corresponding to a loss of function of the G796R mutated protein, in accordance with the heterozygous status of the AE1 variant patients. In conclusion, stopped-flow led to measurement of rapid transport kinetics using the natural substrate for AE1 and, conjugated with flow cytometry, allowed a reliable correlation of chloride/bicarbonate exchange to surface expression of AE1, both in recombinant cells and ghosts and therefore a fine comparison of function between different stomatocytosis samples. This technical approach thus provides significant improvements in anion exchange analysis in red blood cells.

Published
2013

18. TSPO ligands stimulate ZnPPIX transport and ROS accumulation leading to the inhibition of P. falciparum growth in human blood

Author

Marginedas-Freixa, I., primary, Hattab, C., additional, Bouyer, G., additional, Halle, F., additional, Chene, A., additional, Lefevre, S. D., additional, Cambot, M., additional, Cueff, A., additional, Schmitt, M., additional, Gamain, B., additional, Lacapere, J. J., additional, Egee, S., additional, Bihel, F., additional, Le Van Kim, C., additional, and Ostuni, M. A., additional

Published
2016
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20. Specificity and sensitivity of RHD genotyping methods by PCR‐based DNA amplification

Author

I Mouro, Le Van Kim C, Yves Colin, J.-P. Cartron, Y. Brossard, Christiane Bignozzi, and J.T. Aubin

Subjects
Genetics, Genotype, Rho(D) Immune Globulin, Gene Amplification, Intron, DNA, Hematology, Biology, Rh Isoimmunization, Polymerase Chain Reaction, Sensitivity and Specificity, Molecular biology, law.invention, Blotting, Southern, Exon, law, Prenatal Diagnosis, Gene duplication, Humans, Gene, Genotyping, Rh blood group system, Polymerase chain reaction
Abstract

Summary. We have compared the sensitivity and specificity of four PCR methods of RHD gene detection using different sets of primers located in the regions of highest divergence between the RHD and RHCE genes, notably exon 10 (method I), exon 7 (method II), exon 4 (method III) and intron 4 (method IV). Methods I‐III were the most sensitive and gave a detectable signal with D-pos/D-neg mixtures containing only 0.001% D-positive cells. Moreover, method II could detect the equivalent DNA amount present in only three nucleated cells in the assay without hybridization of PCR products, whereas the sensitivity of the other methods was 10‐50 times less. Investigation of D variants indicated that false-negative results were obtained with method II (D IVb variant), method III (D VI and DFR variants) and method IV (D VI variants), but not method I. Weak D (D u ) was correctly detected as D-positive by all methods, but most cases of Rhnull appeared as false-positives, as they carry normal RH genes that are not phenotypically expressed. Some false-positive results were obtained with method I in a few Caucasian DNA samples serotyped as RhD-neg but carrying a C -o r E-allele, whereas a high incidence of false-positives was found among non-Caucasian Rh-negative samples by all methods. In the Caucasian population, however, we found a full correlation between the predicted genotype and observed phenotype at birth of 92 infants. Although we routinely use the four methods for RHD genotyping, a PCR strategy based on at least two methods is recommended.

Published
1997
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23. Test diagnostique d’immunisation contre le VIH aisément applicable en milieu déshérité reposant sur des VHH (dérivés recombinants d’anticorps de camélidés)

Author

Habib, I., primary, Smolarek, D., additional, Hattab, C., additional, Grodecka, M., additional, Gutiérrez, C., additional, Laperche, S., additional, LE-Van-Kim, C., additional, Colin Aronovicz, Y., additional, Wasniowska, K., additional, Gangnard, S., additional, and Bertrand, O., additional

Published
2013
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26. Disruption of a GATA motif in the Duffy gene promoter abolishes erythroid gene expression in Duffy-negative individuals

Author

Christophe Tournamille, J.-P. Cartron, Yves Colin, and Le Van Kim C

Subjects
Erythrocytes, Genotype, Transcription, Genetic, Molecular Sequence Data, Protozoan Proteins, Black People, Gene Expression, Antigens, Protozoan, Receptors, Cell Surface, Biology, Exon, Chemokine receptor, Antigen, Gene expression, Genetics, Tumor Cells, Cultured, Humans, GATA1 Transcription Factor, Promoter Regions, Genetic, Gene, Base Sequence, Chromosome Mapping, GATA1, Promoter, Molecular biology, Chemokine Receptor Gene, DNA-Binding Proteins, Mutation, Erythroid-Specific DNA-Binding Factors, Carrier Proteins, Duffy Blood-Group System, Transcription Factors
Abstract

The mRNA for the Duffy blood group antigen, the erythrocyte receptor for the Plasmodium vivax malaria parasite, has recently been cloned and shown to encode a widely expressed chemokine receptor. Here, we show that the Duffy antigen/chemokine receptor gene (DARC) is composed of a single exon and that most Duffy–negative blacks carry a silent FY*B allele with a single T to C substitution at nucleotide −46. This mutation impairs the promoter activity in erythroid cells by disrupting a binding site for the GATA1 erythroid transcription factor. With the recent characterization of the FY*A and FY*B alleles, these findings provide the molecular basis of the Duffy blood group system and an explanation for the erythroid–speeific repression of the DARC gene in Duffy–negative individuals.

Published
1995

28. VHHs or nanobodies directed against proteins of the human red cell membrane

Author

Smolarek, D., primary, Habib, I., additional, Hattab, C., additional, Cochet, S., additional, Hassanzadeh-Ghassabeh, G., additional, Gutierrez, C., additional, Picot, J., additional, Grodecka, M., additional, Wasniowska, K., additional, Udomsangpetch, R., additional, de Brevern, A.G., additional, Muyldermans, S., additional, Colin, Y., additional, Le Van Kim, C., additional, Czerwinski, M., additional, and Bertrand, O., additional

Published
2010
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31. Papers to be published in forthcoming issues. Toward more effective antifungal therapy: the prospects of combination therapy. Myeloma cells can directly contribute to the pool of RANKL in bone bypassing the classic stromal and osteoblast pathway of osteoc

Author

Kontoyiannis, D. P., primary, Lewis, R. E., additional, Lai, F. P. L., additional, Cole-Sinclair, M., additional, Cheng, W.-J., additional, Quinn, J. M. W., additional, Gillespie, M. T., additional, Sentry, J. W., additional, Schneider, H.-G., additional, Kroft, S. H., additional, Asplund, S. L., additional, McKenna, R. W., additional, Karandikar, N. J., additional, Mannucci, P. M., additional, Capoferri, C., additional, Canciani, M. T., additional, Bord, S., additional, Frith, E., additional, Ireland, D. C., additional, Scott, M. A., additional, Craig, J. I. O., additional, Compston, J. E, additional, Kroviarski, Y., additional, El Nemer, W., additional, Gane, P., additional, Rahuel, C., additional, Gauthier, E., additional, Lecomte, M. C., additional, Cartron, J. P., additional, Colin, Y., additional, Le Van Kim, C., additional, Lee, E., additional, Burgess, G., additional, Halverson, G. R., additional, Huang, T. J., additional, Reid, M. E., additional, Breit, S., additional, Nees, M., additional, Schaefer, U., additional, Pfoersich, M., additional, Hagemeier, C., additional, Muckenthaler, M., additional, Kulozik, A. E., additional, Okada, H., additional, Takagi, A., additional, Murate, T., additional, Adachi, T., additional, Yamamoto, K., additional, Matsushita, T., additional, Takamatsu, J., additional, Sugita, K., additional, Sugimoto, M., additional, Yoshioka, A., additional, Yamazaki, T., additional, Saito, H., additional, and Kojima, T., additional

Published
2004
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