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American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 2015, Volume 192, Issue 8, pp. 983 - 997
Rationale: Inflammation and endothelial dysfunction are considered two primary instigators of pulmonary arterial hypertension (PAH). CD74 is a receptor for the... 
Macrophage migration inhibitory factor | CD74 signaling pathway | Endothelial dysfunction | Adhesion molecules | Pulmonary hypertension | CD74 | RECRUITMENT | macrophage migration inhibitory factor | pulmonary hypertension | PHENOTYPE | MIF | CELL-SURVIVAL | PREVENTS | endothelial dysfunction | FIBROBLAST GROWTH FACTOR-2 | adhesion molecules | RESPIRATORY SYSTEM | ARTERIAL-HYPERTENSION | MICE | CONTRIBUTES | CRITICAL CARE MEDICINE | Leukocytes, Mononuclear - metabolism | Up-Regulation | Humans | Macrophage Migration-Inhibitory Factors - immunology | Middle Aged | Macrophage Migration-Inhibitory Factors - metabolism | Male | Case-Control Studies | Familial Primary Pulmonary Hypertension - metabolism | Pulmonary Artery - metabolism | Familial Primary Pulmonary Hypertension - immunology | Leukocytes, Mononuclear - immunology | Antigens, Differentiation, B-Lymphocyte - immunology | Adult | Female | Histocompatibility Antigens Class II - metabolism | Disease Models, Animal | Endothelium, Vascular - immunology | Vascular Cell Adhesion Molecule-1 - immunology | Signal Transduction | Endothelial Cells - metabolism | Intercellular Adhesion Molecule-1 - immunology | Cells, Cultured | Endothelium, Vascular - physiopathology | Rats | E-Selectin - metabolism | E-Selectin - immunology | Inflammation | Endothelial Cells - immunology | Intercellular Adhesion Molecule-1 - metabolism | Animals | Histocompatibility Antigens Class II - immunology | Endothelium, Vascular - metabolism | Antigens, Differentiation, B-Lymphocyte - metabolism | In Vitro Techniques | Vascular Cell Adhesion Molecule-1 - metabolism | Pulmonary Artery - immunology
Journal Article
Nature Communications, ISSN 2041-1723, 04/2018, Volume 9, Issue 1, pp. 1416 - 16
Pulmonary arterial hypertension (PAH) is a rare disorder with a poor prognosis. Deleterious variation within components of the transforming growth factor-beta... 
a_open_article_in_open_journal | SOX17 | GENE | ANGIOGENESIS | CRYSTAL-STRUCTURE | MULTIDISCIPLINARY SCIENCES | BMP9 | ASSOCIATION | EXPRESSION | NONSENSE MUTATION | BETA-RECEPTOR | CAVEOLIN-1 | Prognosis | Humans | Male | Familial Primary Pulmonary Hypertension - diagnosis | SOXF Transcription Factors - metabolism | Aquaporin 1 - metabolism | Case-Control Studies | Familial Primary Pulmonary Hypertension - metabolism | Membrane Transport Proteins - genetics | Base Sequence | HEK293 Cells | Adult | Female | Growth Differentiation Factors - genetics | Membrane Transport Proteins - metabolism | Familial Primary Pulmonary Hypertension - pathology | Genetic Predisposition to Disease | Bone Morphogenetic Protein Receptors, Type II - genetics | Signal Transduction | Gene Expression Regulation | Adenosine Triphosphatases - metabolism | Models, Molecular | Familial Primary Pulmonary Hypertension - genetics | Bone Morphogenetic Protein Receptors, Type II - metabolism | Membrane Transport Proteins - chemistry | Whole Genome Sequencing | Aquaporin 1 - chemistry | Aquaporin 1 - genetics | Growth Differentiation Factors - metabolism | Transforming Growth Factor beta - genetics | Adenosine Triphosphatases - chemistry | Adenosine Triphosphatases - genetics | Mutation | SOXF Transcription Factors - genetics | Transforming Growth Factor beta - metabolism | SOXF Transcription Factors - chemistry | Growth Differentiation Factors - chemistry | Hypertension | Bone morphogenetic protein receptor type II | Secretion | Transforming growth factor | Genes | Genomes | Heritability | Aquaporin 1 | Gene sequencing
Journal Article
Circulation, ISSN 0009-7322, 12/2017, Volume 136, Issue 25, pp. 2451 - 2467
BACKGROUND: Pulmonary arterial hypertension (PAH) is characterized by abnormal growth and enhanced glycolysis of pulmonary artery endothelial cells. However,... 
microRNAs | hypertension, pulmonary | endothelial cells | metabolism | endothelial progenitor cells | glycolysis | APOPTOSIS | COACTIVATOR | CARDIAC & CARDIOVASCULAR SYSTEMS | hypertension pulmonary | TUMOR | INHIBITION | MIR-124 | GROWTH | PERIPHERAL VASCULAR DISEASE | EXPRESSION | Cell Proliferation | MicroRNAs - antagonists & inhibitors | Humans | MicroRNAs - metabolism | Polypyrimidine Tract-Binding Protein - antagonists & inhibitors | Familial Primary Pulmonary Hypertension - metabolism | Lim Kinases - metabolism | Monocarboxylic Acid Transporters - metabolism | RNA Interference | Smad5 Protein - metabolism | Bone Morphogenetic Protein Receptors, Type II - antagonists & inhibitors | Disease Models, Animal | Familial Primary Pulmonary Hypertension - pathology | Bone Morphogenetic Protein Receptors, Type II - genetics | Pyruvate Kinase - metabolism | Endothelial Cells - metabolism | Cells, Cultured | Heterogeneous-Nuclear Ribonucleoproteins - metabolism | Rats | Familial Primary Pulmonary Hypertension - genetics | Heterogeneous-Nuclear Ribonucleoproteins - antagonists & inhibitors | Polypyrimidine Tract-Binding Protein - metabolism | Bone Morphogenetic Protein Receptors, Type II - metabolism | Symporters - metabolism | Heterogeneous-Nuclear Ribonucleoproteins - genetics | Animals | Endothelial Cells - cytology | Glycolysis | Smad1 Protein - metabolism | MicroRNAs - genetics | Antagomirs - metabolism | Pyruvate Kinase - genetics | Polypyrimidine Tract-Binding Protein - genetics | RNA, Small Interfering - metabolism
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 05/2018, Volume 128, Issue 5, pp. 1956 - 1970
Pulmonary arterial hypertension (PAH) is characterized by a progressive accumulation of pulmonary artery smooth muscle cells (PA-SMCs) in pulmonary arterioles... 
MEDICINE, RESEARCH & EXPERIMENTAL | FIBROBLAST GROWTH FACTOR-2 | INTERLEUKIN-6 RECEPTOR | OVEREXPRESSION | SMOOTH-MUSCLE-CELLS | MICE | CYTOKINE | BMPR-II | CONTRIBUTES | IL-6 RECEPTOR | BETA | Familial Primary Pulmonary Hypertension - pathology | Up-Regulation | Vascular Remodeling | Muscle, Smooth, Vascular - metabolism | Humans | Myocytes, Smooth Muscle - pathology | Rats | Familial Primary Pulmonary Hypertension - genetics | Mice, Transgenic | Pulmonary Artery - physiopathology | Signal Transduction - genetics | Muscle, Smooth, Vascular - physiopathology | Familial Primary Pulmonary Hypertension - metabolism | Familial Primary Pulmonary Hypertension - physiopathology | Arterioles - pathology | Muscle, Smooth, Vascular - pathology | Pulmonary Artery - metabolism | Animals | Arterioles - metabolism | Arterioles - physiopathology | Cytokine Receptor gp130 - biosynthesis | Mice | Myocytes, Smooth Muscle - metabolism | Pulmonary Artery - pathology | Care and treatment | Cytokine receptors | Physiological aspects | Development and progression | Health aspects | Pulmonary artery | Pulmonary hypertension | Interleukin-6 | Cytochrome | Hypertension | Animal models | Cytokines | Arterioles | Pathogenesis | Pulmonary arteries | Smooth muscle | Cardiovascular disease | Interleukin 6 | Proteins | Signal transduction | Interleukin 6 receptors | Rodents | Medical prognosis | Hypoxia | Heart diseases | Growth factors | Glycoprotein gp130 | Veins & arteries
Journal Article
Circulation, ISSN 0009-7322, 10/2016, Volume 134, Issue 15, pp. 1105 - 1121
Journal Article
Cardiovascular Research, ISSN 0008-6363, 2016, Volume 111, Issue 1, pp. 16 - 25
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 06/2017, Volume 37, Issue 8, pp. 1559 - 1569
OBJECTIVE—We determined in patients with pulmonary arterial (PA) hypertension (PAH) whether in addition to increased production of elastase by PA smooth muscle... 
smooth muscle cells | TGF-beta-1 | fibroblasts | BMPR2 receptor | hypertension, pulmonary | fibrillin-1 | elastin | BMPR2 | ENDOTHELIAL DYSFUNCTION | FIBRILLIN | IN-VITRO | GENE | MARFAN-SYNDROME | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | MICE | MUTATIONS | HEMATOLOGY | EXPRESSION | Vascular Remodeling | Humans | Myocytes, Smooth Muscle - pathology | Hypertension, Pulmonary - physiopathology | Mice, 129 Strain | Case-Control Studies | Familial Primary Pulmonary Hypertension - metabolism | Familial Primary Pulmonary Hypertension - physiopathology | Elastic Tissue - metabolism | Pulmonary Artery - metabolism | Transfection | RNA Interference | Bone Morphogenetic Protein Receptors, Type I - deficiency | Fibrillin-1 - metabolism | Fibrillin-1 - genetics | Myocytes, Smooth Muscle - drug effects | Myocytes, Smooth Muscle - metabolism | Disease Models, Animal | Fibroblasts - metabolism | Familial Primary Pulmonary Hypertension - pathology | Elastin - metabolism | Genetic Predisposition to Disease | Bone Morphogenetic Protein Receptors, Type II - genetics | Mice, Inbred C57BL | Bone Morphogenetic Protein Receptors, Type II - deficiency | Cells, Cultured | Bone Morphogenetic Protein Receptors, Type I - genetics | Familial Primary Pulmonary Hypertension - genetics | Hypertension, Pulmonary - genetics | Hypertension, Pulmonary - metabolism | Pulmonary Artery - physiopathology | Elastic Tissue - physiopathology | Pulmonary Artery - drug effects | Fibroblasts - pathology | Bone Morphogenetic Protein 4 - pharmacology | Bone Morphogenetic Protein Receptors, Type II - metabolism | Mice, Knockout | Elastic Tissue - pathology | Transforming Growth Factor beta - pharmacology | Phenotype | Animals | Elastin - genetics | Fibroblasts - drug effects | Mutation | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology
Journal Article
FEBS Letters, ISSN 0014-5793, 01/2016, Volume 590, Issue 1, pp. 101 - 109
Pulmonary arterial hypertension (PAH) is characterized by excessive pulmonary arterial smooth muscle cells (PASMCs) growth, partially in response to PDGF‐BB... 
smooth muscle cells | Wnt signaling | vascular remodeling | pulmonary disease | PDGF | pulmonary hypertension | Proto-Oncogene Proteins c-sis - chemistry | Muscle, Smooth, Vascular - metabolism | Humans | Glycogen Synthase Kinase 3 beta | Wnt-5a Protein | Promoter Regions, Genetic - drug effects | Wnt Proteins - metabolism | Familial Primary Pulmonary Hypertension - metabolism | Pulmonary Artery - metabolism | Wnt Proteins - genetics | Protein Processing, Post-Translational - drug effects | RNA Interference | Phosphorylation - drug effects | Proto-Oncogene Proteins c-sis - pharmacology | Muscle, Smooth, Vascular - drug effects | Familial Primary Pulmonary Hypertension - pathology | Proto-Oncogene Proteins - metabolism | Recombinant Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-sis - metabolism | beta Catenin - agonists | Cells, Cultured | Proto-Oncogene Proteins - genetics | Pulmonary Artery - drug effects | Recombinant Proteins - pharmacology | Glycogen Synthase Kinase 3 - metabolism | Muscle, Smooth, Vascular - cytology | beta Catenin - metabolism | beta Catenin - genetics | Pulmonary Artery - cytology | Gene Expression Regulation - drug effects | Muscle, Smooth, Vascular - pathology | Wnt Signaling Pathway - drug effects | beta Catenin - antagonists & inhibitors | Active Transport, Cell Nucleus - drug effects | Anticoagulants - pharmacology | Genes, Reporter - drug effects | Cell Proliferation - drug effects | Wnt Proteins - antagonists & inhibitors | Pulmonary Artery - pathology
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 09/2016, Volume 36, Issue 9, pp. 1879 - 1890
Journal Article
PLoS ONE, ISSN 1932-6203, 06/2014, Volume 9, Issue 6, p. e100310
Mutations affecting transforming growth factor-beta (TGF-beta) superfamily receptors, activin receptor-like kinase (ALK)-1, and endoglin (ENG) occur in... 
CELLS | LUNG | GROWTH-FACTOR-BETA | INHIBITION | SMOOTH-MUSCLE HYPERPLASIA | BONE MORPHOGENETIC PROTEIN | MULTIDISCIPLINARY SCIENCES | ARTERIAL-HYPERTENSION | MUTATION | PROLIFERATION | EXPRESSION | Endothelium, Vascular - cytology | Activin Receptors, Type II - metabolism | Phosphorylation | Receptors, Transforming Growth Factor beta - genetics | Cell Proliferation | Prognosis | Follow-Up Studies | Humans | Male | Case-Control Studies | Familial Primary Pulmonary Hypertension - metabolism | Immunoenzyme Techniques | Endoglin | Pulmonary Artery - metabolism | Female | Real-Time Polymerase Chain Reaction | Familial Primary Pulmonary Hypertension - pathology | Enzyme-Linked Immunosorbent Assay | Signal Transduction | Mice, Inbred C57BL | RNA, Messenger - genetics | Cells, Cultured | Familial Primary Pulmonary Hypertension - genetics | Hypertension, Pulmonary - genetics | Hypertension, Pulmonary - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Mice, Knockout | Pulmonary Artery - cytology | Animals | Transforming Growth Factor beta - genetics | Receptors, Transforming Growth Factor beta - metabolism | Endothelium, Vascular - metabolism | Activin Receptors, Type II - genetics | Mice | Intracellular Signaling Peptides and Proteins - physiology | Hypertension, Pulmonary - pathology | Transforming Growth Factor beta - metabolism | Heart | Systolic pressure | Endothelin | Pathogenesis | Transforming growth factor-b | Interleukin | Smooth muscle | Kinases | Macrophages | Interleukin 6 | Signal transduction | Receptors | Cell growth | Rodents | Smad2 protein | Blood pressure | Growth factors | Hypertension | Fibroblast growth factor 2 | Cytokines | Incubation | Muscles | Blood vessels | Inflammation | Patients | Pulmonary artery | Endothelial cells | Signaling | Lungs | Monocyte chemoattractant protein | Hypoxia | Infiltration | Ventricle | Mutation | Activin | Monocyte chemoattractant protein 1 | Hypertrophy | Veins & arteries
Journal Article