Arthritis & Rheumatology, ISSN 2326-5191, 02/2015, Volume 67, Issue 2, pp. 517 - 526
Objective Fli‐1, a potential predisposing factor for systemic sclerosis (SSc), is constitutively down‐regulated in the lesional skin of patients with SSc by an...
GROWTH-FACTOR-BETA | SCLERODERMA FIBROBLASTS | INCREASED EXPRESSION | COLLAGEN FIBRILLOGENESIS | DERMAL FIBROBLASTS | ANIMAL-MODEL | PROTEIN-ASSOCIATED FACTOR | RHEUMATOLOGY | MESENCHYMAL TRANSITION | TRANSCRIPTION FACTOR FLI1 | INTEGRIN ALPHA-V-BETA-5 | Skin - metabolism | Epithelial-Mesenchymal Transition - physiology | Scleroderma, Systemic - pathology | Integrins - metabolism | Cell Movement - physiology | Mice, Mutant Strains | Scleroderma, Systemic - physiopathology | Female | Proto-Oncogene Protein c-fli-1 - deficiency | Skin - pathology | Disease Models, Animal | Haploinsufficiency - genetics | Cytokines - metabolism | Macrophages - pathology | Proto-Oncogene Protein c-fli-1 - genetics | Mice, Inbred C57BL | Endothelium, Vascular - physiopathology | Proto-Oncogene Protein c-fli-1 - physiology | Immune System - pathology | Bleomycin - adverse effects | Scleroderma, Systemic - chemically induced | Animals | Immune System - physiopathology | Mast Cells - pathology | Fibrosis | Endothelium, Vascular - pathology | Mice | Transforming Growth Factor beta - metabolism | Medical research | Rodents | Cell adhesion & migration
GROWTH-FACTOR-BETA | SCLERODERMA FIBROBLASTS | INCREASED EXPRESSION | COLLAGEN FIBRILLOGENESIS | DERMAL FIBROBLASTS | ANIMAL-MODEL | PROTEIN-ASSOCIATED FACTOR | RHEUMATOLOGY | MESENCHYMAL TRANSITION | TRANSCRIPTION FACTOR FLI1 | INTEGRIN ALPHA-V-BETA-5 | Skin - metabolism | Epithelial-Mesenchymal Transition - physiology | Scleroderma, Systemic - pathology | Integrins - metabolism | Cell Movement - physiology | Mice, Mutant Strains | Scleroderma, Systemic - physiopathology | Female | Proto-Oncogene Protein c-fli-1 - deficiency | Skin - pathology | Disease Models, Animal | Haploinsufficiency - genetics | Cytokines - metabolism | Macrophages - pathology | Proto-Oncogene Protein c-fli-1 - genetics | Mice, Inbred C57BL | Endothelium, Vascular - physiopathology | Proto-Oncogene Protein c-fli-1 - physiology | Immune System - pathology | Bleomycin - adverse effects | Scleroderma, Systemic - chemically induced | Animals | Immune System - physiopathology | Mast Cells - pathology | Fibrosis | Endothelium, Vascular - pathology | Mice | Transforming Growth Factor beta - metabolism | Medical research | Rodents | Cell adhesion & migration
Journal Article
Nature Communications, ISSN 2041-1723, 2014, Volume 5, Issue 1, p. 5797
Systemic sclerosis (SSc) is manifested by fibrosis, vasculopathy and immune dysregulation. So far, a unifying hypothesis underpinning these pathological events...
GROWTH-FACTOR-BETA | DNA-BINDING | PULMONARY ARTERIAL-HYPERTENSION | MULTIDISCIPLINARY SCIENCES | COLLAGEN FIBRILLOGENESIS | TISSUE FIBROSIS | GENE-EXPRESSION | PROTEIN-ASSOCIATED FACTOR | DISEASE SCLERODERMA | TRANSCRIPTION FACTOR FLI1 | AUTOIMMUNE-DISEASE | Autoimmunity | RNA, Small Interfering - genetics | Skin - metabolism | Blood Vessels - metabolism | Blood Vessels - pathology | Connective Tissue Growth Factor - immunology | Epigenesis, Genetic | Humans | Scleroderma, Systemic - pathology | Autoantibodies - biosynthesis | Case-Control Studies | Blood Vessels - immunology | Collagen - genetics | Lung - metabolism | B-Lymphocytes - pathology | B-Lymphocytes - metabolism | Skin - pathology | Disease Models, Animal | Fibroblasts - metabolism | Skin - immunology | Lung - pathology | Proto-Oncogene Protein c-fli-1 - genetics | Signal Transduction | Lymphocyte Activation | Collagen - immunology | Scleroderma, Systemic - metabolism | Scleroderma, Systemic - genetics | Mice, Transgenic | Connective Tissue Growth Factor - agonists | Scleroderma, Systemic - immunology | Fibroblasts - pathology | Proto-Oncogene Protein c-fli-1 - antagonists & inhibitors | Animals | B-Lymphocytes - immunology | Fibrosis | Fibroblasts - immunology | Collagen - agonists | Connective Tissue Growth Factor - genetics | Mice | Kruppel-Like Transcription Factors - antagonists & inhibitors | Kruppel-Like Transcription Factors - genetics | Kruppel-Like Transcription Factors - immunology | Lung - immunology | Proto-Oncogene Protein c-fli-1 - immunology | RNA, Small Interfering - metabolism
GROWTH-FACTOR-BETA | DNA-BINDING | PULMONARY ARTERIAL-HYPERTENSION | MULTIDISCIPLINARY SCIENCES | COLLAGEN FIBRILLOGENESIS | TISSUE FIBROSIS | GENE-EXPRESSION | PROTEIN-ASSOCIATED FACTOR | DISEASE SCLERODERMA | TRANSCRIPTION FACTOR FLI1 | AUTOIMMUNE-DISEASE | Autoimmunity | RNA, Small Interfering - genetics | Skin - metabolism | Blood Vessels - metabolism | Blood Vessels - pathology | Connective Tissue Growth Factor - immunology | Epigenesis, Genetic | Humans | Scleroderma, Systemic - pathology | Autoantibodies - biosynthesis | Case-Control Studies | Blood Vessels - immunology | Collagen - genetics | Lung - metabolism | B-Lymphocytes - pathology | B-Lymphocytes - metabolism | Skin - pathology | Disease Models, Animal | Fibroblasts - metabolism | Skin - immunology | Lung - pathology | Proto-Oncogene Protein c-fli-1 - genetics | Signal Transduction | Lymphocyte Activation | Collagen - immunology | Scleroderma, Systemic - metabolism | Scleroderma, Systemic - genetics | Mice, Transgenic | Connective Tissue Growth Factor - agonists | Scleroderma, Systemic - immunology | Fibroblasts - pathology | Proto-Oncogene Protein c-fli-1 - antagonists & inhibitors | Animals | B-Lymphocytes - immunology | Fibrosis | Fibroblasts - immunology | Collagen - agonists | Connective Tissue Growth Factor - genetics | Mice | Kruppel-Like Transcription Factors - antagonists & inhibitors | Kruppel-Like Transcription Factors - genetics | Kruppel-Like Transcription Factors - immunology | Lung - immunology | Proto-Oncogene Protein c-fli-1 - immunology | RNA, Small Interfering - metabolism
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 04/2017, Volume 214, Issue 4, pp. 1129 - 1151
Systemic sclerosis (SSc), or scleroderma, is a multisystem autoimmune disorder characterized by vasculopathy and fibrosis in the skin and internal organs, most...
MEDICINE, RESEARCH & EXPERIMENTAL | DIGITAL ULCERS | AIRE | GENE-EXPRESSION PATTERNS | DOWN-REGULATION | CD4(+) T-CELLS | DISEASE SCLERODERMA | SKIN | IMMUNOLOGY | TRANSCRIPTION FACTOR | SCLEROSIS PATIENTS | DERMAL FIBROSIS | Autoimmunity | Th17 Cells - physiology | Transcription Factors - physiology | Th2 Cells - physiology | Humans | Transcriptome | Keratin-14 - analysis | Proto-Oncogene Protein c-fli-1 - physiology | Transcription Factors - genetics | Epithelial Cells - physiology | Esophagus - pathology | Animals | Scleroderma, Systemic - etiology | Keratinocytes - metabolism | Fibrosis | Mice | Homeodomain Proteins - physiology | Skin - pathology | Disease Models, Animal | Transcription factors | Pathogenesis | Epithelial cells | Leukemia | Viruses | Mimicry | Thymus | Keratin | Vascular diseases | Rodents | Fibroblasts | Scleroderma | Immune system | Lung diseases | Organs | Keratinocytes | Esophagus | Gene silencing | Lungs | Systemic sclerosis | Skin | AIRE protein | Autoimmune diseases | Auditory defects | 300
MEDICINE, RESEARCH & EXPERIMENTAL | DIGITAL ULCERS | AIRE | GENE-EXPRESSION PATTERNS | DOWN-REGULATION | CD4(+) T-CELLS | DISEASE SCLERODERMA | SKIN | IMMUNOLOGY | TRANSCRIPTION FACTOR | SCLEROSIS PATIENTS | DERMAL FIBROSIS | Autoimmunity | Th17 Cells - physiology | Transcription Factors - physiology | Th2 Cells - physiology | Humans | Transcriptome | Keratin-14 - analysis | Proto-Oncogene Protein c-fli-1 - physiology | Transcription Factors - genetics | Epithelial Cells - physiology | Esophagus - pathology | Animals | Scleroderma, Systemic - etiology | Keratinocytes - metabolism | Fibrosis | Mice | Homeodomain Proteins - physiology | Skin - pathology | Disease Models, Animal | Transcription factors | Pathogenesis | Epithelial cells | Leukemia | Viruses | Mimicry | Thymus | Keratin | Vascular diseases | Rodents | Fibroblasts | Scleroderma | Immune system | Lung diseases | Organs | Keratinocytes | Esophagus | Gene silencing | Lungs | Systemic sclerosis | Skin | AIRE protein | Autoimmune diseases | Auditory defects | 300
Journal Article
PLOS ONE, ISSN 1932-6203, 05/2019, Volume 14, Issue 5, p. e0216358
The interaction between high-mobility group box 1 protein (HMGB1) and receptor for advanced glycation end products (RAGE) is important for tumor cell growth....
MALIGNANT GLIOMA | MULTIDISCIPLINARY SCIENCES | GROWTH | CYCLE ARREST | HMGB1 | BLOOD-BRAIN-BARRIER | DISCOVERY | Antimitotic agents | Product development | Antineoplastic agents | Drug therapy | Papaverine | Glioblastoma multiforme | Cell proliferation | Cell culture | Brain cancer | Xenotransplantation | Glioblastoma | Smooth muscle | Oncology | Biochemistry | Neurosurgery | Drug development | HMGB1 protein | Cancer therapies | Hemorrhage | Cell adhesion & migration | Anticancer properties | Biological effects | Cell growth | Xenografts | Cell cycle | DNA methylation | Supplementation | Pharmaceutical sciences | Deoxyribonucleic acid--DNA | Medical research | Advanced glycosylation end products | Muscle relaxants | Narcotics | Muscles | Breast cancer | Glycosylation | Radiation therapy | Medicine | Chemotherapy | Brain research | Inhibitors | In vivo methods and tests | Glioblastoma cells | Temozolomide | Cell migration | Tumors | Apoptosis | Deoxyribonucleic acid | DNA
MALIGNANT GLIOMA | MULTIDISCIPLINARY SCIENCES | GROWTH | CYCLE ARREST | HMGB1 | BLOOD-BRAIN-BARRIER | DISCOVERY | Antimitotic agents | Product development | Antineoplastic agents | Drug therapy | Papaverine | Glioblastoma multiforme | Cell proliferation | Cell culture | Brain cancer | Xenotransplantation | Glioblastoma | Smooth muscle | Oncology | Biochemistry | Neurosurgery | Drug development | HMGB1 protein | Cancer therapies | Hemorrhage | Cell adhesion & migration | Anticancer properties | Biological effects | Cell growth | Xenografts | Cell cycle | DNA methylation | Supplementation | Pharmaceutical sciences | Deoxyribonucleic acid--DNA | Medical research | Advanced glycosylation end products | Muscle relaxants | Narcotics | Muscles | Breast cancer | Glycosylation | Radiation therapy | Medicine | Chemotherapy | Brain research | Inhibitors | In vivo methods and tests | Glioblastoma cells | Temozolomide | Cell migration | Tumors | Apoptosis | Deoxyribonucleic acid | DNA
Journal Article
Arthritis & Rheumatology, ISSN 2326-5191, 01/2015, Volume 67, Issue 1, pp. 254 - 265
Objective Bleomycin‐induced fibrosis and the tight skin (TSK/+) mouse are well‐established experimental murine models of human systemic sclerosis (SSc)....
LUNG FIBROSIS | TIGHT-SKIN | IMMUNE-RESPONSES | SERUM-LEVELS | REGULATES SKIN | RHEUMATOLOGY | AUTOIMMUNE-DISEASE | BLEOMYCIN-INDUCED SCLERODERMA | PULMONARY-FIBROSIS | CLINICAL-SIGNIFICANCE | INNATE IMMUNITY | Cytokines - metabolism | Mice, Inbred C57BL | Toll-Like Receptor 4 - genetics | Bleomycin - adverse effects | Mice, Knockout | Scleroderma, Systemic - chemically induced | Toll-Like Receptor 4 - physiology | Animals | Toll-Like Receptor 4 - deficiency | Scleroderma, Systemic - physiopathology | Female | Neovascularization, Pathologic - physiopathology | Signal Transduction - physiology | Mice | Fibrosis - pathology | Fibrosis - prevention & control | Scleroderma, Systemic - prevention & control | Skin - pathology | Disease Models, Animal | Medical research | Rodents | Immune system
LUNG FIBROSIS | TIGHT-SKIN | IMMUNE-RESPONSES | SERUM-LEVELS | REGULATES SKIN | RHEUMATOLOGY | AUTOIMMUNE-DISEASE | BLEOMYCIN-INDUCED SCLERODERMA | PULMONARY-FIBROSIS | CLINICAL-SIGNIFICANCE | INNATE IMMUNITY | Cytokines - metabolism | Mice, Inbred C57BL | Toll-Like Receptor 4 - genetics | Bleomycin - adverse effects | Mice, Knockout | Scleroderma, Systemic - chemically induced | Toll-Like Receptor 4 - physiology | Animals | Toll-Like Receptor 4 - deficiency | Scleroderma, Systemic - physiopathology | Female | Neovascularization, Pathologic - physiopathology | Signal Transduction - physiology | Mice | Fibrosis - pathology | Fibrosis - prevention & control | Scleroderma, Systemic - prevention & control | Skin - pathology | Disease Models, Animal | Medical research | Rodents | Immune system
Journal Article
Arthritis & Rheumatology, ISSN 2326-5191, 05/2015, Volume 67, Issue 5, pp. 1335 - 1344
Objective It is generally accepted that blockade of endothelin receptors has potentially beneficial effects on vasculopathy associated with systemic sclerosis...
GROWTH-FACTOR-BETA | SCLERODERMA FIBROBLASTS | DIGITAL ULCERS | DEFICIENCY CONTRIBUTES | DERMAL FIBROBLASTS | PROTEIN-ASSOCIATED FACTOR | RHEUMATOLOGY | SYSTEMIC-SCLEROSIS | TRANSCRIPTION FACTOR FLI1 | EXPRESSION | BOSENTAN REVERSES | Immunohistochemistry | Phosphorylation | Capillary Permeability | Humans | Actins - metabolism | Immunoblotting | RNA, Messenger - metabolism | Chromatin Immunoprecipitation | Proto-Oncogene Protein c-fli-1 - metabolism | Vascular Diseases | Microvessels - cytology | Cell Line | Promoter Regions, Genetic | Gene Expression | Proto-Oncogene Protein c-fli-1 - genetics | Endothelial Cells - metabolism | Endothelin-1 - metabolism | Scleroderma, Systemic - metabolism | Cells, Cultured | Receptors, Endothelin - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Sulfonamides - pharmacology | Mice, Knockout | Protein Kinase C-delta - metabolism | Endothelin Receptor Antagonists - pharmacology | Animals | Proto-Oncogene Proteins c-abl - metabolism | Mice | Proteins | Kinases | Rodents | Deoxyribonucleic acid--DNA
GROWTH-FACTOR-BETA | SCLERODERMA FIBROBLASTS | DIGITAL ULCERS | DEFICIENCY CONTRIBUTES | DERMAL FIBROBLASTS | PROTEIN-ASSOCIATED FACTOR | RHEUMATOLOGY | SYSTEMIC-SCLEROSIS | TRANSCRIPTION FACTOR FLI1 | EXPRESSION | BOSENTAN REVERSES | Immunohistochemistry | Phosphorylation | Capillary Permeability | Humans | Actins - metabolism | Immunoblotting | RNA, Messenger - metabolism | Chromatin Immunoprecipitation | Proto-Oncogene Protein c-fli-1 - metabolism | Vascular Diseases | Microvessels - cytology | Cell Line | Promoter Regions, Genetic | Gene Expression | Proto-Oncogene Protein c-fli-1 - genetics | Endothelial Cells - metabolism | Endothelin-1 - metabolism | Scleroderma, Systemic - metabolism | Cells, Cultured | Receptors, Endothelin - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Sulfonamides - pharmacology | Mice, Knockout | Protein Kinase C-delta - metabolism | Endothelin Receptor Antagonists - pharmacology | Animals | Proto-Oncogene Proteins c-abl - metabolism | Mice | Proteins | Kinases | Rodents | Deoxyribonucleic acid--DNA
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2015, Volume 112, Issue 49, pp. 15136 - 15141
Systemic sclerosis (SSc) is a multisystem autoimmune disorder with clinical manifestations resulting from tissue fibrosis and extensive vasculopathy. A...
Vasculopathy | Interferon regulatory factor 5 | Systemic sclerosis | Fibrosis | Toll-like receptor 4 | FUNCTIONAL POLYMORPHISM | MULTIDISCIPLINARY SCIENCES | interferon regulatory factor 5 | RECEPTOR 4 | FLI1 | SCLERODERMA | systemic sclerosis | INFLAMMATION | DISEASE | fibrosis | vasculopathy | ASSOCIATION | CLINICAL-SIGNIFICANCE | Toll-Like Receptor 4 - physiology | Animals | B-Lymphocytes - immunology | Lymphocyte Activation | Mice, Inbred C57BL | Scleroderma, Systemic - physiopathology | Interferon Regulatory Factors - genetics | Interferon Regulatory Factors - physiology | Female | Mice | Mice, Knockout | Care and treatment | Transcription factors | Systemic scleroderma | Patient outcomes | Scleroderma (Disease) | Development and progression | Research | Risk factors | Biological Sciences
Vasculopathy | Interferon regulatory factor 5 | Systemic sclerosis | Fibrosis | Toll-like receptor 4 | FUNCTIONAL POLYMORPHISM | MULTIDISCIPLINARY SCIENCES | interferon regulatory factor 5 | RECEPTOR 4 | FLI1 | SCLERODERMA | systemic sclerosis | INFLAMMATION | DISEASE | fibrosis | vasculopathy | ASSOCIATION | CLINICAL-SIGNIFICANCE | Toll-Like Receptor 4 - physiology | Animals | B-Lymphocytes - immunology | Lymphocyte Activation | Mice, Inbred C57BL | Scleroderma, Systemic - physiopathology | Interferon Regulatory Factors - genetics | Interferon Regulatory Factors - physiology | Female | Mice | Mice, Knockout | Care and treatment | Transcription factors | Systemic scleroderma | Patient outcomes | Scleroderma (Disease) | Development and progression | Research | Risk factors | Biological Sciences
Journal Article
Arthritis & Rheumatology, ISSN 2326-5191, 09/2017, Volume 69, Issue 9, pp. 1879 - 1890
Objective To determine the function and serum levels of soluble forms of programmed death 1 (sPD‐1) and one of its ligands, soluble PD ligand 2 (sPD‐L2), in...
LUNG FIBROSIS | SCLERODERMA | B-CELL | AUTOIMMUNITY | T-CELL-ACTIVATION | RECEPTOR | SKIN | RHEUMATOLOGY | PD-1 | ASSOCIATION | EXPRESSION | Severity of Illness Index | Scleroderma, Systemic - blood | Enzyme-Linked Immunosorbent Assay | Humans | Middle Aged | DNA Topoisomerases, Type I | Scleroderma, Systemic - pathology | Male | Programmed Cell Death 1 Ligand 2 Protein - blood | Programmed Cell Death 1 Receptor - blood | Disease Progression | Macrophages - metabolism | Animals | Flow Cytometry | Scleroderma, Systemic - etiology | T-Lymphocytes - metabolism | Adult | Female | Mice | B-Lymphocytes - metabolism | Lymphocyte receptors | Flow cytometry | PD-1 protein | Interleukin | Lymphocytes T | Macrophages | Lymphocytes | Rodents | Enzyme-linked immunosorbent assay | Recombinant | Cytokines | Abnormalities | Mortality | DNA topoisomerase | Cultures | Patients | Serum levels | Cytometry | Lymphocytes B | Systemic sclerosis | Interleukin 10 | Fibrosis | Ligands | Death | Apoptosis
LUNG FIBROSIS | SCLERODERMA | B-CELL | AUTOIMMUNITY | T-CELL-ACTIVATION | RECEPTOR | SKIN | RHEUMATOLOGY | PD-1 | ASSOCIATION | EXPRESSION | Severity of Illness Index | Scleroderma, Systemic - blood | Enzyme-Linked Immunosorbent Assay | Humans | Middle Aged | DNA Topoisomerases, Type I | Scleroderma, Systemic - pathology | Male | Programmed Cell Death 1 Ligand 2 Protein - blood | Programmed Cell Death 1 Receptor - blood | Disease Progression | Macrophages - metabolism | Animals | Flow Cytometry | Scleroderma, Systemic - etiology | T-Lymphocytes - metabolism | Adult | Female | Mice | B-Lymphocytes - metabolism | Lymphocyte receptors | Flow cytometry | PD-1 protein | Interleukin | Lymphocytes T | Macrophages | Lymphocytes | Rodents | Enzyme-linked immunosorbent assay | Recombinant | Cytokines | Abnormalities | Mortality | DNA topoisomerase | Cultures | Patients | Serum levels | Cytometry | Lymphocytes B | Systemic sclerosis | Interleukin 10 | Fibrosis | Ligands | Death | Apoptosis
Journal Article
Arthritis Research and Therapy, ISSN 1478-6354, 02/2018, Volume 20, Issue 1, pp. 23 - 11
Background: Friend leukemia virus integration 1 (Fli1) deficiency, a predisposing factor of systemic sclerosis (SSc), induces SSc-like phenotypes in various...
Fibroblasts | Regulatory T cells | IL-33 | Systemic sclerosis | Fli1 | DNA-BINDING | TGF-BETA | DOWN-REGULATION | RHEUMATOLOGY | SYSTEMIC-SCLEROSIS | BLEOMYCIN-INDUCED SCLERODERMA | ANIMAL-MODEL | MICE | EXPRESSION | FLI1 DEFICIENCY CONTRIBUTES | TH17 CELLS | T-Lymphocytes, Regulatory - metabolism | Dermis - metabolism | Proto-Oncogene Protein c-fli-1 - genetics | Skin - metabolism | Coculture Techniques | Mice, Inbred C57BL | Scleroderma, Systemic - metabolism | Cells, Cultured | Scleroderma, Systemic - genetics | Cell Transdifferentiation - genetics | Th2 Cells - metabolism | Haploinsufficiency | Mice, Knockout | Animals | Proto-Oncogene Protein c-fli-1 - metabolism | Cell Transdifferentiation - drug effects | Cell Communication - drug effects | Interleukin-33 - metabolism | Bleomycin - pharmacology | Female | Fibroblasts - metabolism | Phenotype | Care and treatment | Systemic scleroderma | Scleroderma (Disease) | Development and progression | Genetic aspects | Health aspects
Fibroblasts | Regulatory T cells | IL-33 | Systemic sclerosis | Fli1 | DNA-BINDING | TGF-BETA | DOWN-REGULATION | RHEUMATOLOGY | SYSTEMIC-SCLEROSIS | BLEOMYCIN-INDUCED SCLERODERMA | ANIMAL-MODEL | MICE | EXPRESSION | FLI1 DEFICIENCY CONTRIBUTES | TH17 CELLS | T-Lymphocytes, Regulatory - metabolism | Dermis - metabolism | Proto-Oncogene Protein c-fli-1 - genetics | Skin - metabolism | Coculture Techniques | Mice, Inbred C57BL | Scleroderma, Systemic - metabolism | Cells, Cultured | Scleroderma, Systemic - genetics | Cell Transdifferentiation - genetics | Th2 Cells - metabolism | Haploinsufficiency | Mice, Knockout | Animals | Proto-Oncogene Protein c-fli-1 - metabolism | Cell Transdifferentiation - drug effects | Cell Communication - drug effects | Interleukin-33 - metabolism | Bleomycin - pharmacology | Female | Fibroblasts - metabolism | Phenotype | Care and treatment | Systemic scleroderma | Scleroderma (Disease) | Development and progression | Genetic aspects | Health aspects
Journal Article
Anticancer Research, ISSN 0250-7005, 12/2019, Volume 39, Issue 12, pp. 6743 - 6750
Journal Article
The Journal of Dermatology, ISSN 0385-2407, 02/2018, Volume 45, Issue 2, pp. 182 - 188
Heparin‐binding epidermal growth factor (EGF)‐like growth factor (HB‐EGF) is a member of the EGF family growth factors, which affects multiple aspects of the...
wound healing | heparin‐binding epidermal growth factor‐like growth factor | systemic sclerosis | inflammation | interstitial lung disease | heparin-binding epidermal growth factor-like growth factor | SCLERODERMA | CLASSIFICATION | PULMONARY-FIBROSIS | FLI1 | CLINICAL-SIGNIFICANCE | DERMATOLOGY | Heparin-binding EGF-like Growth Factor - genetics | Scleroderma, Systemic - blood | Skin - cytology | Humans | Middle Aged | Scleroderma, Systemic - pathology | Male | Pulmonary Fibrosis - blood | Lung - diagnostic imaging | RNA, Messenger - metabolism | Pulmonary Fibrosis - diagnostic imaging | Heparin-binding EGF-like Growth Factor - blood | Fibroblasts | Adult | Female | Skin - pathology | Scleroderma, Systemic - diagnostic imaging | Lung - pathology | Cells, Cultured | Pulmonary Fibrosis - pathology | Heparin-binding EGF-like Growth Factor - metabolism | Biopsy | Fibrosis | Mucin-1 - blood | Aged | Respiratory Function Tests | Transforming Growth Factor beta - metabolism | Respiratory tract diseases | Anticoagulants (Medicine) | Epidermal growth factor | Systemic scleroderma | Scleroderma (Disease) | Wound healing | Transforming growth factor-b | Lung diseases | mRNA | Inflammation | Small intestine | Contraction | Angiogenesis | Heparin-binding epidermal growth factor-like growth factor | Systemic sclerosis | Skin diseases | Heparin | Growth factors
wound healing | heparin‐binding epidermal growth factor‐like growth factor | systemic sclerosis | inflammation | interstitial lung disease | heparin-binding epidermal growth factor-like growth factor | SCLERODERMA | CLASSIFICATION | PULMONARY-FIBROSIS | FLI1 | CLINICAL-SIGNIFICANCE | DERMATOLOGY | Heparin-binding EGF-like Growth Factor - genetics | Scleroderma, Systemic - blood | Skin - cytology | Humans | Middle Aged | Scleroderma, Systemic - pathology | Male | Pulmonary Fibrosis - blood | Lung - diagnostic imaging | RNA, Messenger - metabolism | Pulmonary Fibrosis - diagnostic imaging | Heparin-binding EGF-like Growth Factor - blood | Fibroblasts | Adult | Female | Skin - pathology | Scleroderma, Systemic - diagnostic imaging | Lung - pathology | Cells, Cultured | Pulmonary Fibrosis - pathology | Heparin-binding EGF-like Growth Factor - metabolism | Biopsy | Fibrosis | Mucin-1 - blood | Aged | Respiratory Function Tests | Transforming Growth Factor beta - metabolism | Respiratory tract diseases | Anticoagulants (Medicine) | Epidermal growth factor | Systemic scleroderma | Scleroderma (Disease) | Wound healing | Transforming growth factor-b | Lung diseases | mRNA | Inflammation | Small intestine | Contraction | Angiogenesis | Heparin-binding epidermal growth factor-like growth factor | Systemic sclerosis | Skin diseases | Heparin | Growth factors
Journal Article
Arthritis & Rheumatology, ISSN 2326-5191, 12/2015, Volume 67, Issue 12, pp. 3245 - 3255
Objective Progranulin is a growth factor that is active in wound repair and is an antagonist of tumor necrosis factor (TNF) receptors, regulating fibroblast...
COLLAGEN PRODUCTION | GROWTH-FACTOR-BETA | SCLERODERMA FIBROBLASTS | TGF-BETA | INCREASED EXPRESSION | DOWN-REGULATION | GRANULIN-EPITHELIN PRECURSOR | PROTEIN-ASSOCIATED FACTOR | RHEUMATOLOGY | TRANSCRIPTION FACTOR FLI1 | FACTOR-ALPHA | Scleroderma, Diffuse - metabolism | Up-Regulation | Humans | Middle Aged | Male | RNA, Messenger - metabolism | Case-Control Studies | Scleroderma, Diffuse - genetics | Gene Knockdown Techniques | Intercellular Signaling Peptides and Proteins - metabolism | Female | Dermis - cytology | Fibroblasts - metabolism | RNA, Messenger - drug effects | Dermis - metabolism | Enzyme-Linked Immunosorbent Assay | Proto-Oncogene Protein c-fli-1 - genetics | Scleroderma, Systemic - metabolism | Gene Expression Regulation | Intercellular Signaling Peptides and Proteins - genetics | Scleroderma, Systemic - genetics | Reverse Transcriptase Polymerase Chain Reaction | Tumor Necrosis Factor-alpha - pharmacology | Animals | Fibroblasts - drug effects | Aged | Mice | Skin | Gangrene | Fibroblasts | Tumor necrosis factor-TNF
COLLAGEN PRODUCTION | GROWTH-FACTOR-BETA | SCLERODERMA FIBROBLASTS | TGF-BETA | INCREASED EXPRESSION | DOWN-REGULATION | GRANULIN-EPITHELIN PRECURSOR | PROTEIN-ASSOCIATED FACTOR | RHEUMATOLOGY | TRANSCRIPTION FACTOR FLI1 | FACTOR-ALPHA | Scleroderma, Diffuse - metabolism | Up-Regulation | Humans | Middle Aged | Male | RNA, Messenger - metabolism | Case-Control Studies | Scleroderma, Diffuse - genetics | Gene Knockdown Techniques | Intercellular Signaling Peptides and Proteins - metabolism | Female | Dermis - cytology | Fibroblasts - metabolism | RNA, Messenger - drug effects | Dermis - metabolism | Enzyme-Linked Immunosorbent Assay | Proto-Oncogene Protein c-fli-1 - genetics | Scleroderma, Systemic - metabolism | Gene Expression Regulation | Intercellular Signaling Peptides and Proteins - genetics | Scleroderma, Systemic - genetics | Reverse Transcriptase Polymerase Chain Reaction | Tumor Necrosis Factor-alpha - pharmacology | Animals | Fibroblasts - drug effects | Aged | Mice | Skin | Gangrene | Fibroblasts | Tumor necrosis factor-TNF
Journal Article
The Journal of Dermatology, ISSN 0385-2407, 07/2016, Volume 43, Issue 7, pp. 808 - 810
Systemic sclerosis (SSc) is believed to be caused by a complex interplay between genetic factors and environmental influences. Although silicone has been...
environmental factor | systemic sclerosis | silicone breast implant | anti‐RNA polymerase III antibody | chronic inflammation | anti-RNA polymerase III antibody | Breast Implants - adverse effects | Humans | Middle Aged | Adult | Female | Male | Silicones - adverse effects | Aged | Scleroderma, Systemic - immunology | RNA Polymerase III - immunology | Viral antibodies | Care and treatment | Systemic scleroderma | RNA | Implants, Artificial | Prosthesis | Scleroderma (Disease) | Antibodies | Silicones | RNA polymerases | Transplants & implants | RNA polymerase
environmental factor | systemic sclerosis | silicone breast implant | anti‐RNA polymerase III antibody | chronic inflammation | anti-RNA polymerase III antibody | Breast Implants - adverse effects | Humans | Middle Aged | Adult | Female | Male | Silicones - adverse effects | Aged | Scleroderma, Systemic - immunology | RNA Polymerase III - immunology | Viral antibodies | Care and treatment | Systemic scleroderma | RNA | Implants, Artificial | Prosthesis | Scleroderma (Disease) | Antibodies | Silicones | RNA polymerases | Transplants & implants | RNA polymerase
Journal Article
The Journal of Dermatology, ISSN 0385-2407, 05/2015, Volume 42, Issue 5, pp. 524 - 527
Patients with systemic sclerosis (SSc) have an increased risk of malignancy compared with the general population. Recently, SSc patients with anti‐RNA...
systemic sclerosis | malignancy | synchronous onset | anti‐RNA polymerase III antibody | Japanese | anti-RNA polymerase III antibody | SCLERODERMA | DISEASE | POPULATION-BASED COHORT | CANCER | DERMATOLOGY | DNA Topoisomerases, Type I - immunology | Japan - epidemiology | Scleroderma, Systemic - blood | Neoplasms - ethnology | Antibodies, Antinuclear - blood | Humans | Middle Aged | Female | Male | RNA Polymerase III - immunology | Neoplasms - epidemiology | Incidence | Autoimmunity | Viral antibodies | Antibodies | Systemic scleroderma | RNA | Scleroderma (Disease)
systemic sclerosis | malignancy | synchronous onset | anti‐RNA polymerase III antibody | Japanese | anti-RNA polymerase III antibody | SCLERODERMA | DISEASE | POPULATION-BASED COHORT | CANCER | DERMATOLOGY | DNA Topoisomerases, Type I - immunology | Japan - epidemiology | Scleroderma, Systemic - blood | Neoplasms - ethnology | Antibodies, Antinuclear - blood | Humans | Middle Aged | Female | Male | RNA Polymerase III - immunology | Neoplasms - epidemiology | Incidence | Autoimmunity | Viral antibodies | Antibodies | Systemic scleroderma | RNA | Scleroderma (Disease)
Journal Article