IL6 receptor blockade preserves articular cartilage and increases bone volume following ischemic osteonecrosis in immature mice.
Identifieur interne : 000C20 ( Main/Exploration ); précédent : 000C19; suivant : 000C21IL6 receptor blockade preserves articular cartilage and increases bone volume following ischemic osteonecrosis in immature mice.
Auteurs : N. Kamiya [Japon] ; G. Kuroyanagi [États-Unis] ; O. Aruwajoye [États-Unis] ; H K W. Kim [États-Unis]Source :
- Osteoarthritis and cartilage [ 1522-9653 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux, Anticorps monoclonaux humanisés (pharmacologie), Anticorps monoclonaux humanisés (usage thérapeutique), Cartilage articulaire (), Cartilage articulaire (anatomopathologie), Cartilage articulaire (métabolisme), Cellules cultivées, Chondrocytes (), Chondrocytes (anatomopathologie), Facteur de transcription SOX-9 (génétique), Facteur de transcription SOX-9 (métabolisme), Fémur (anatomopathologie), Fémur (métabolisme), Interleukine-6 (métabolisme), Microtomographie aux rayons X, Modèles animaux de maladie humaine, Métabolisme (), Ostéonécrose (anatomopathologie), Ostéonécrose (traitement médicamenteux), Remodelage osseux (), Récepteurs à l'interleukine-6 (antagonistes et inhibiteurs), Récepteurs à l'interleukine-6 (physiologie), Régulation positive (), Souris de lignée C57BL, Thérapie moléculaire ciblée (), Évaluation préclinique de médicament ().
- MESH :
- anatomopathologie : Cartilage articulaire, Chondrocytes, Fémur, Ostéonécrose.
- antagonistes et inhibiteurs : Récepteurs à l'interleukine-6.
- génétique : Facteur de transcription SOX-9.
- métabolisme : Cartilage articulaire, Facteur de transcription SOX-9, Fémur, Interleukine-6.
- pharmacologie : Anticorps monoclonaux humanisés.
- physiologie : Récepteurs à l'interleukine-6.
- traitement médicamenteux : Ostéonécrose.
- usage thérapeutique : Anticorps monoclonaux humanisés.
- Animaux, Cartilage articulaire, Cellules cultivées, Chondrocytes, Microtomographie aux rayons X, Modèles animaux de maladie humaine, Métabolisme, Remodelage osseux, Régulation positive, Souris de lignée C57BL, Thérapie moléculaire ciblée, Évaluation préclinique de médicament.
English descriptors
- KwdEn :
- Animals, Antibodies, Monoclonal, Humanized (pharmacology), Antibodies, Monoclonal, Humanized (therapeutic use), Bone Remodeling (drug effects), Cartilage, Articular (drug effects), Cartilage, Articular (metabolism), Cartilage, Articular (pathology), Cells, Cultured, Chondrocytes (drug effects), Chondrocytes (pathology), Disease Models, Animal, Drug Evaluation, Preclinical (methods), Femur (metabolism), Femur (pathology), Interleukin-6 (metabolism), Metabolism (drug effects), Mice, Inbred C57BL, Molecular Targeted Therapy (methods), Osteonecrosis (drug therapy), Osteonecrosis (pathology), Receptors, Interleukin-6 (antagonists & inhibitors), Receptors, Interleukin-6 (physiology), SOX9 Transcription Factor (genetics), SOX9 Transcription Factor (metabolism), Up-Regulation (drug effects), X-Ray Microtomography.
- MESH :
- chemical , antagonists & inhibitors : Receptors, Interleukin-6.
- chemical , genetics : SOX9 Transcription Factor.
- chemical , metabolism : Interleukin-6, SOX9 Transcription Factor.
- chemical , pharmacology : Antibodies, Monoclonal, Humanized.
- chemical , physiology : Receptors, Interleukin-6.
- chemical , therapeutic use : Antibodies, Monoclonal, Humanized.
- drug effects : Bone Remodeling, Cartilage, Articular, Chondrocytes, Metabolism, Up-Regulation.
- drug therapy : Osteonecrosis.
- metabolism : Cartilage, Articular, Femur.
- methods : Drug Evaluation, Preclinical, Molecular Targeted Therapy.
- pathology : Cartilage, Articular, Chondrocytes, Femur, Osteonecrosis.
- Animals, Cells, Cultured, Disease Models, Animal, Mice, Inbred C57BL, X-Ray Microtomography.
Abstract
Juvenile ischemic osteonecrosis (JIO) of the femoral head is one of the most serious hip disorders causing a permanent deformity of the femoral head in childhood. We recently reported that interleukin 6 (IL6) is predominantly increased in the hip synovial fluid of patients with JIO and that articular chondrocytes are primary source of IL6. This study investigated whether an inhibition of IL6 receptor improves cartilage preservation and bone healing in JIO.
DOI: 10.1016/j.joca.2018.10.010
PubMed: 30404032
Affiliations:
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Le document en format XML
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<term>Antibodies, Monoclonal, Humanized (therapeutic use)</term>
<term>Bone Remodeling (drug effects)</term>
<term>Cartilage, Articular (drug effects)</term>
<term>Cartilage, Articular (metabolism)</term>
<term>Cartilage, Articular (pathology)</term>
<term>Cells, Cultured</term>
<term>Chondrocytes (drug effects)</term>
<term>Chondrocytes (pathology)</term>
<term>Disease Models, Animal</term>
<term>Drug Evaluation, Preclinical (methods)</term>
<term>Femur (metabolism)</term>
<term>Femur (pathology)</term>
<term>Interleukin-6 (metabolism)</term>
<term>Metabolism (drug effects)</term>
<term>Mice, Inbred C57BL</term>
<term>Molecular Targeted Therapy (methods)</term>
<term>Osteonecrosis (drug therapy)</term>
<term>Osteonecrosis (pathology)</term>
<term>Receptors, Interleukin-6 (antagonists & inhibitors)</term>
<term>Receptors, Interleukin-6 (physiology)</term>
<term>SOX9 Transcription Factor (genetics)</term>
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<term>Anticorps monoclonaux humanisés (usage thérapeutique)</term>
<term>Cartilage articulaire ()</term>
<term>Cartilage articulaire (anatomopathologie)</term>
<term>Cartilage articulaire (métabolisme)</term>
<term>Cellules cultivées</term>
<term>Chondrocytes ()</term>
<term>Chondrocytes (anatomopathologie)</term>
<term>Facteur de transcription SOX-9 (génétique)</term>
<term>Facteur de transcription SOX-9 (métabolisme)</term>
<term>Fémur (anatomopathologie)</term>
<term>Fémur (métabolisme)</term>
<term>Interleukine-6 (métabolisme)</term>
<term>Microtomographie aux rayons X</term>
<term>Modèles animaux de maladie humaine</term>
<term>Métabolisme ()</term>
<term>Ostéonécrose (anatomopathologie)</term>
<term>Ostéonécrose (traitement médicamenteux)</term>
<term>Remodelage osseux ()</term>
<term>Récepteurs à l'interleukine-6 (antagonistes et inhibiteurs)</term>
<term>Récepteurs à l'interleukine-6 (physiologie)</term>
<term>Régulation positive ()</term>
<term>Souris de lignée C57BL</term>
<term>Thérapie moléculaire ciblée ()</term>
<term>Évaluation préclinique de médicament ()</term>
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<term>Ostéonécrose</term>
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<term>Cartilage, Articular</term>
<term>Chondrocytes</term>
<term>Metabolism</term>
<term>Up-Regulation</term>
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<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Osteonecrosis</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur de transcription SOX-9</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cartilage, Articular</term>
<term>Femur</term>
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<term>Facteur de transcription SOX-9</term>
<term>Fémur</term>
<term>Interleukine-6</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cartilage, Articular</term>
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<term>Osteonecrosis</term>
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<term>Cartilage articulaire</term>
<term>Cellules cultivées</term>
<term>Chondrocytes</term>
<term>Microtomographie aux rayons X</term>
<term>Modèles animaux de maladie humaine</term>
<term>Métabolisme</term>
<term>Remodelage osseux</term>
<term>Régulation positive</term>
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<front><div type="abstract" xml:lang="en">Juvenile ischemic osteonecrosis (JIO) of the femoral head is one of the most serious hip disorders causing a permanent deformity of the femoral head in childhood. We recently reported that interleukin 6 (IL6) is predominantly increased in the hip synovial fluid of patients with JIO and that articular chondrocytes are primary source of IL6. This study investigated whether an inhibition of IL6 receptor improves cartilage preservation and bone healing in JIO.</div>
</front>
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