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Circulation Research, ISSN 0009-7330, 03/2009, Volume 104, Issue 6, pp. 733 - 741
Vascular calcification is a major risk factor for cardiovascular morbidity and mortality. To develop appropriate prevention and/or therapeutic strategies for... 
Vascular calcification | Smooth muscle cells | Genetic fate mapping | Lineage reprogramming | Runx2/Cbfa1 | WALL | CARDIAC & CARDIOVASCULAR SYSTEMS | vascular calcification | ATHEROSCLEROSIS | lineage reprogramming | genetic fate mapping | CARTILAGE | smooth muscle cells | IN-VITRO | DEFICIENT | CALCIFICATION | PERIPHERAL VASCULAR DISEASE | MICE | MUTATIONS | MATRIX-GLA-PROTEIN | HEMATOLOGY | EXPRESSION | Calcinosis - genetics | Vascular Diseases - pathology | Homeodomain Proteins - metabolism | Humans | Myocytes, Smooth Muscle - pathology | Extracellular Signal-Regulated MAP Kinases - metabolism | RNA, Messenger - metabolism | Stem Cells - metabolism | Wnt Proteins - metabolism | Core Binding Factor Alpha 1 Subunit - metabolism | Extracellular Signal-Regulated MAP Kinases - genetics | Arteries - metabolism | MAP Kinase Signaling System - genetics | Wnt Proteins - genetics | Mice, Mutant Strains | Bone Morphogenetic Protein 2 - metabolism | Calcinosis - metabolism | Myocytes, Smooth Muscle - metabolism | Chondrocytes - metabolism | SOX9 Transcription Factor - metabolism | Bone Morphogenetic Protein 2 - genetics | Chondrocytes - pathology | RNA, Messenger - genetics | Vascular Diseases - genetics | Arteries - pathology | Transcription Factors - genetics | Down-Regulation - genetics | Homeodomain Proteins - genetics | Mice, Knockout | Proteins - genetics | Transcription Factors - metabolism | Animals | Proteins - metabolism | Sp7 Transcription Factor | Stem Cells - pathology | Wnt3 Protein | Mice | Calcinosis - pathology | Vascular Diseases - metabolism | Wnt3A Protein | Cell Dedifferentiation - genetics | SOX9 Transcription Factor - genetics | Core Binding Factor Alpha 1 Subunit - genetics | Index Medicus | Cbfa1 | Runx2
Journal Article
Nature, ISSN 0028-0836, 2013, Volume 499, Issue 7459, pp. 491 - 495
The tyrosine phosphatase SHP2, encoded by PTPN11, is required for the survival, proliferation and differentiation of various cell types(1,2). Germline... 
ENCHONDROMATOSIS | RANVIER | OSTEOCLASTS | MULTIDISCIPLINARY SCIENCES | OSSIFICATION GROOVE | PERICHONDRIAL RING | CELL PROLIFERATION | RECEPTOR | OSTEOGENESIS | CHONDROGENESIS | CARTILAGE | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Cartilage - pathology | Hedgehog Proteins - metabolism | Monocytes - metabolism | Bone Neoplasms - pathology | Bone Neoplasms - metabolism | MAP Kinase Signaling System | Fibroblast Growth Factors - metabolism | Mitogen-Activated Protein Kinase Kinases - metabolism | Mesenchymal Stromal Cells - cytology | Cell Division | Gene Deletion | Genes, Tumor Suppressor - physiology | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - deficiency | Exostoses, Multiple Hereditary - genetics | Bone Neoplasms - genetics | Bone Neoplasms - drug therapy | Osteopetrosis - genetics | Osteopetrosis - pathology | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Exostoses, Multiple Hereditary - metabolism | Mesenchymal Stromal Cells - metabolism | Mice, Transgenic | Osteopetrosis - metabolism | Chondromatosis - metabolism | Hedgehog Proteins - antagonists & inhibitors | Cartilage - metabolism | Osteoclasts - metabolism | Parathyroid Hormone-Related Protein - metabolism | Exostoses, Multiple Hereditary - pathology | Mice, Knockout | Exostoses, Multiple Hereditary - drug therapy | Gene Expression Regulation - drug effects | Cell Lineage | Cathepsin K - genetics | Macrophages - metabolism | Animals | Chondromatosis - drug therapy | Cathepsin K - metabolism | Chondromatosis - genetics | Signal Transduction - drug effects | Chondromatosis - pathology | Mice | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics | Cathepsin K - deficiency | Tyrosine | Phosphatases | Physiological aspects | Cellular signal transduction | Research | Bone diseases | Health aspects | Hedgehog proteins | Flow cytometry | Pathogenesis | Rodents | Bone density | Mutation | Kinases | Gene expression | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 1/2013, Volume 110, Issue 5, pp. 1875 - 1880
Here we examined the involvement of Notch signaling in the endochondral ossification process, which is crucial for osteoarthritis (OA) development.... 
Cartilage | Knee joint | Articular cartilage | Chondrocytes | Ligands | Bones | Mice | Skeletal development | Gene expression regulation | Osteoarthritis | Cartilage degradation | CELLS | OSTEOBLAST DIFFERENTIATION | MULTIDISCIPLINARY SCIENCES | skeletal development | BONE-DEVELOPMENT | KNEE-JOINT INSTABILITY | LIGANDS | ARTICULAR-CARTILAGE | PATHWAY | GROWTH | cartilage degradation | EXPERIMENTAL MOUSE MODELS | EXPRESSION | Cartilage - pathology | Homeodomain Proteins - metabolism | Humans | Cartilage - drug effects | Collagen Type II - metabolism | Knee Joint - pathology | Basic Helix-Loop-Helix Transcription Factors - metabolism | Serrate-Jagged Proteins | Immunoglobulin J Recombination Signal Sequence-Binding Protein - genetics | Jagged-1 Protein | SOX9 Transcription Factor - metabolism | Basic Helix-Loop-Helix Transcription Factors - genetics | Signal Transduction | Membrane Proteins - genetics | Osteoarthritis - metabolism | Mice, Transgenic | Reverse Transcriptase Polymerase Chain Reaction | Mice, Knockout | Cell Line, Tumor | HeLa Cells | Receptor, Notch1 - antagonists & inhibitors | Receptor, Notch1 - genetics | Calcium-Binding Proteins - genetics | Transcription Factor HES-1 | Receptor, Notch2 - antagonists & inhibitors | Receptor, Notch2 - genetics | Chondrocytes - drug effects | Intercellular Signaling Peptides and Proteins - metabolism | Membrane Proteins - metabolism | Chondrocytes - metabolism | Calcium-Binding Proteins - metabolism | Knee Joint - metabolism | Cell Line | Immunoglobulin J Recombination Signal Sequence-Binding Protein - metabolism | Osteoarthritis - prevention & control | Dipeptides - pharmacology | Knee Joint - drug effects | Mice, Inbred C57BL | Intercellular Signaling Peptides and Proteins - genetics | Receptor, Notch2 - metabolism | Receptor, Notch1 - metabolism | Cartilage - metabolism | Collagen Type II - genetics | Homeodomain Proteins - genetics | Osteoarthritis - genetics | Animals | Fluorescent Antibody Technique | SOX9 Transcription Factor - genetics | Osteogenesis | Endochondral ossification | Physiological aspects | Development and progression | Cellular signal transduction | Health aspects | Membrane proteins | Proteins | Knee | Tissue | Rodents | Arthritis | Cells | Index Medicus | Biological Sciences
Journal Article
Arteriosclerosis Thrombosis and Vascular Biology, ISSN 1079-5642, 02/2015, Volume 35, Issue 2, pp. 399 - 408
OBJECTIVE—Vascular and valvular calcifications are pathological processes regulated by resident cells, and depending on a complex interplay between... 
aortic valve | multivesicular bodies | calcification of | gene expression | vascular calcification | AORTIC-STENOSIS | MATRIX VESICLES | VALVE | aortic valve, calcification of | CARTILAGE | DISEASE | VITAMIN-K | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | EXPRESSION | FETUIN-A | INSIGHTS | Calcinosis - genetics | Aortic Valve Stenosis - genetics | Calcium - metabolism | Humans | Middle Aged | Vascular Calcification - genetics | Actins - metabolism | Osteocalcin - genetics | Male | Aorta - metabolism | Case-Control Studies | Aortic Valve - pathology | Coronary Vessels - metabolism | Aortic Valve Stenosis - prevention & control | Vascular Calcification - metabolism | Coronary Artery Disease - pathology | Aged, 80 and over | Adult | Female | Calcinosis - metabolism | Extracellular Matrix Proteins - metabolism | Calcium-Binding Proteins - metabolism | Coronary Vessels - pathology | Osteocalcin - metabolism | Tissue Culture Techniques | Coronary Artery Disease - metabolism | Extracellular Matrix Proteins - genetics | Coronary Artery Disease - prevention & control | Gene Expression Regulation | Vascular Calcification - prevention & control | Vascular Calcification - pathology | Aortic Valve - metabolism | Aorta - pathology | Proteins - genetics | Aortic Valve Stenosis - pathology | Proteins - metabolism | Coronary Artery Disease - genetics | alpha-2-HS-Glycoprotein - metabolism | Aortic Valve Stenosis - metabolism | Aged | Calcinosis - prevention & control | Calcinosis - pathology | Calcium-Binding Proteins - genetics | Index Medicus
Journal Article
Nature Medicine, ISSN 1078-8956, 12/2011, Volume 17, Issue 12, pp. 1674 - 1679
Journal Article
Osteoarthritis and Cartilage, ISSN 1063-4584, 2015, Volume 24, Issue 2, pp. 315 - 324
Summary Objective The aetiology of OA is not fully understood although several adipokines such as leptin are known mediators of disease progression. Since... 
Rheumatology | Smad1 | Human chondrocytes | Hip osteoarthritis | β-Catenin | Dedifferentiation | Leptin | COLLAGEN | RHEUMATOLOGY | DIFFERENTIATED PHENOTYPE | HYPERTROPHY | IN-VITRO | SYNOVIAL FIBROBLASTS | HUMAN OSTEOARTHRITIC CARTILAGE | SIGNALING PATHWAY | beta-Catenin | ARTICULAR CHONDROCYTES | ORTHOPEDICS | KNEE OSTEOARTHRITIS | EXPRESSION | Receptors, Transforming Growth Factor beta - genetics | Humans | Leptin - metabolism | Middle Aged | Male | Lymphotoxin-alpha - metabolism | RNA, Messenger - metabolism | Core Binding Factor Alpha 1 Subunit - metabolism | Lymphotoxin-alpha - genetics | Cartilage, Articular - metabolism | Smad5 Protein - metabolism | Smad2 Protein - genetics | Aged, 80 and over | Smad2 Protein - drug effects | Protein-Serine-Threonine Kinases - metabolism | Collagen Type X - drug effects | SOX9 Transcription Factor - metabolism | Matrix Metalloproteinase 13 - genetics | Smad2 Protein - metabolism | Prednisolone - pharmacology | beta Catenin - metabolism | Matrix Metalloproteinase 13 - metabolism | Glycogen Synthase Kinase 3 - genetics | Receptors, Transforming Growth Factor beta - drug effects | Activin Receptors, Type II - genetics | Protein-Serine-Threonine Kinases - drug effects | Activin Receptors, Type II - metabolism | Osteoarthritis, Hip - metabolism | Glycogen Synthase Kinase 3 - drug effects | Activin Receptors, Type II - drug effects | Chondrocytes - drug effects | Collagen Type X - metabolism | beta Catenin - drug effects | Smad1 Protein - genetics | Adult | Female | Smad5 Protein - genetics | Chondrocytes - metabolism | RNA, Messenger - drug effects | Cell Dedifferentiation - drug effects | Cartilage, Articular - cytology | Lymphotoxin-alpha - drug effects | Protein-Serine-Threonine Kinases - genetics | Collagen Type X - genetics | SOX9 Transcription Factor - drug effects | Matrix Metalloproteinase 13 - drug effects | Glycogen Synthase Kinase 3 - metabolism | beta Catenin - genetics | Osteoarthritis, Hip - genetics | Smad5 Protein - drug effects | Core Binding Factor Alpha 1 Subunit - drug effects | Wnt Signaling Pathway - drug effects | Receptors, Transforming Growth Factor beta - metabolism | Wnt Signaling Pathway - genetics | Glucocorticoids - pharmacology | Smad1 Protein - metabolism | Aged | Smad1 Protein - drug effects | Cartilage, Articular - drug effects | In Vitro Techniques | Cell Dedifferentiation - genetics | Core Binding Factor Alpha 1 Subunit - genetics | Index Medicus
Journal Article
Archives of Oral Biology, ISSN 0003-9969, 02/2019, Volume 98, pp. 17 - 25
To investigate the changes in insulin-like growth factor-1 (IGF-1) expression levels in the degenerative mandibular condylar cartilage. Thirty-six rats were... 
Temporomandibular joint | Insulin-like growth factor-1 (IGF-1) | Articular cartilage | Chondrocyte | Osteoarthritis | Dental occlusion | IGF-I | PERICELLULAR MATRIX | ALKALINE-PHOSPHATASE | BINDING-PROTEINS | CHONDROCYTE HYPERTROPHY | ARTICULAR-CARTILAGE | TEMPOROMANDIBULAR-JOINT | DENTISTRY, ORAL SURGERY & MEDICINE | DEGRADATION | PLATE | EXPRESSION | Receptor, IGF Type 1 - metabolism | Up-Regulation | Alkaline Phosphatase - metabolism | Glucuronidase - metabolism | Malocclusion - complications | Gene Expression Profiling | ADAMTS5 Protein - metabolism | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Insulin-Like Growth Factor Binding Protein 3 - metabolism | Mandibular Condyle - pathology | Tissue Inhibitor of Metalloproteinase-3 - metabolism | Female | Insulin-Like Growth Factor Binding Protein 5 - metabolism | Cartilage Diseases - etiology | Disease Models, Animal | Chondrocytes - pathology | Rats | Matrix Metalloproteinase 3 - metabolism | ADAMTS4 Protein - metabolism | Aggrecans - metabolism | Rats, Sprague-Dawley | Matrix Metalloproteinase 13 - metabolism | Gene Expression Regulation, Enzymologic | Cartilage, Articular - pathology | Collagen - metabolism | Animals | Temporomandibular Joint Disorders - etiology | Mandibular Condyle - metabolism | Proliferating Cell Nuclear Antigen - metabolism | Insulin-Like Growth Factor I - metabolism | Index Medicus | Dentistry
Journal Article
Osteoarthritis and Cartilage, ISSN 1063-4584, 2015, Volume 23, Issue 12, pp. 2288 - 2296
Summary Objective Hypoxia-inducible factor-2α (HIF-2α) transcriptionally upregulates Nampt in articular chondrocytes. NAMPT, which exhibits nicotinamide... 
Rheumatology | NAD+ biosynthesis | Hypoxia-inducible factor (HIF) | Sirtuin | Osteoarthritis | Chondrocytes | NAD | biosynthesis | APOPTOSIS | RHEUMATOLOGY | SIRTUINS | NAD(+) biosynthesis | SIRT1 | CARTILAGE | NUCLEUS PULPOSUS CELLS | METABOLISM | BIOLOGY | GROWTH | STRESS | ORTHOPEDICS | EXPRESSION | Sirtuin 1 - metabolism | Up-Regulation | Arthritis, Experimental - genetics | Immunoprecipitation | Matrix Metalloproteinase 12 - genetics | RNA, Messenger - metabolism | Sirtuin 1 - genetics | Arthritis, Experimental - metabolism | Sirtuin 2 - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Nicotinamide Phosphoribosyltransferase - metabolism | Cartilage, Articular - metabolism | Sirtuins - genetics | Cytokines - genetics | Chondrocytes - metabolism | NAD - metabolism | Basic Helix-Loop-Helix Transcription Factors - genetics | Cytokines - metabolism | Matrix Metalloproteinase 13 - genetics | Matrix Metalloproteinase 3 - metabolism | Matrix Metalloproteinase 12 - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Matrix Metalloproteinase 13 - metabolism | Sirtuin 2 - genetics | Nicotinamide Phosphoribosyltransferase - genetics | Animals | Osteoarthritis, Knee - genetics | Mice | Matrix Metalloproteinase 3 - genetics | Sirtuins - metabolism | Osteoarthritis, Knee - metabolism | Index Medicus
Journal Article
Matrix Biology, ISSN 0945-053X, 2011, Volume 30, Issue 2, pp. 145 - 153
Aggrecan degradation in articular cartilage occurs predominantly through proteolysis and has been attributed to the action of members of the matrix... 
MMP | ADAMTS | Interglobular domain | Chondroitin-sulfate-2 region | Aggrecan catabolism | RHEUMATOID-ARTHRITIS | PROTEOLYTIC CLEAVAGE | CLEAVAGE SITE | ACTIVATION MECHANISMS | LARGE AGGREGATING PROTEOGLYCAN | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL BIOLOGY | HUMAN ARTICULAR-CARTILAGE | MATRIX METALLOPROTEINASES | OSTEOARTHRITIC CARTILAGE | ONCOSTATIN-M | Matrix Metalloproteinases, Secreted - metabolism | Interleukin-1beta - pharmacology | Phenylmercuric Acetate - pharmacology | Matrix Metalloproteinase 12 - genetics | Cartilage - drug effects | Oncostatin M - pharmacology | Matrix Metalloproteinase 9 - metabolism | Matrix Metalloproteinase 7 - metabolism | Cattle | Isoenzymes - metabolism | Matrix Metalloproteinase 8 - metabolism | Gelatinases - metabolism | Matrix Metalloproteinase 1 - genetics | Recombinant Proteins - metabolism | Endopeptidases - metabolism | Matrix Metalloproteinase 8 - genetics | Peptide Fragments - metabolism | Isoenzymes - genetics | Matrix Metalloproteinase 2 - metabolism | Matrix Metalloproteinase 3 - metabolism | Aggrecans - metabolism | Matrix Metalloproteinase 12 - metabolism | Cartilage - metabolism | Aggrecans - genetics | ADAM Proteins - metabolism | Enzyme Precursors - metabolism | Matrix Metalloproteinase 7 - genetics | Animals | Endopeptidases - genetics | Matrix Metalloproteinases, Secreted - genetics | Phenylmercuric Acetate - analogs & derivatives | ADAM Proteins - genetics | Cartilage - enzymology | Matrix Metalloproteinase 1 - metabolism | Matrix Metalloproteinase 3 - genetics | Index Medicus
Journal Article
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 03/2013, Volume 17, Issue 3, pp. 365 - 376
The role of hydrogen sulfide ( H 2 S ) in inflammation remains unclear with both pro‐ and anti‐inflammatory actions of this gas described. We have now assessed... 
GYY | synoviocyte | myeloperoxidase | COX | TNF | 2 | hydrogen sulfide | inflammation | Freund's adjuvant | 4137 | cytokines | alpha converting enzyme | lipopolysaccharide | GYY4137 | Hydrogen sulfide | Synoviocyte | COX-2 | Cytokines | Lipopolysaccharide | Myeloperoxidase | Inflammation | TNF-alpha converting enzyme | MEDICINE, RESEARCH & EXPERIMENTAL | RAT | VIVO | NITRIC-OXIDE SYNTHASE | MACROPHAGES | MEDIATOR | LUNG INJURY | CELL BIOLOGY | HEMORRHAGIC-SHOCK | RESPONSES | IN-VITRO | INHIBITION | Hydrogen Sulfide - metabolism | Tumor Necrosis Factor-alpha - metabolism | Arthritis - metabolism | Cartilage - pathology | Humans | Synovial Membrane - pathology | NF-kappa B - metabolism | Cartilage - drug effects | Synovial Membrane - drug effects | Organothiophosphorus Compounds - pharmacology | Chondrocytes - drug effects | Inflammation - metabolism | Inflammation - drug therapy | Inflammation Mediators - metabolism | Arthritis - etiology | Chondrocytes - metabolism | Joints - metabolism | Disease Models, Animal | Fibroblasts - metabolism | Chondrocytes - pathology | Acute Disease | Cytokines - metabolism | Enzyme-Linked Immunosorbent Assay | Joints - drug effects | Cells, Cultured | Morpholines - pharmacology | Joints - pathology | Cartilage - metabolism | Fibroblasts - pathology | Inflammation - etiology | Synovial Membrane - metabolism | Animals | Fibroblasts - drug effects | Arthritis - drug therapy | Cyclooxygenase 2 - metabolism | Lipopolysaccharides - pharmacology | Mice | Nitric Oxide Synthase Type II - metabolism | COX-2 inhibitors | Enzymes | Analysis | Nitric oxide | Mitogens | Cartilage | Rodents | Effects | Joints | Inflammatory diseases | Index Medicus | Original
Journal Article