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American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 05/2017, Volume 56, Issue 5, pp. 597 - 608
Monocytes/macrophages are major effectors of lung inflammation associated with various forms of pulmonary hypertension ( PH). Interactions between the... 
Monocytes | Macrophages | Chemokines | Pulmonary hypertension | CX3CL1/CX3CR1 and CCL2/CCR2 | CX3CR1 | FRACTALKINE | monocytes | pulmonary hypertension | BIOCHEMISTRY & MOLECULAR BIOLOGY | ATHEROSCLEROSIS | chemokines | DEFICIENCY | CELL BIOLOGY | macrophages | REPAIR | INHIBITION | RESPIRATORY SYSTEM | INFLAMMATION | ARTERIAL-HYPERTENSION | CCR5 | Lung - pathology | Chemokine CX3CL1 - metabolism | Mice, Inbred C57BL | Receptors, Chemokine - metabolism | Myocytes, Smooth Muscle - pathology | Male | Monocytes - metabolism | Hypertension, Pulmonary - metabolism | Hypoxia - complications | Hypoxia - metabolism | Macrophages - metabolism | Phenotype | Receptors, CCR2 - metabolism | Animals | Gene Deletion | Ligands | Chemokine CCL2 - metabolism | CX3C Chemokine Receptor 1 | Myocytes, Smooth Muscle - metabolism | Pulmonary Artery - pathology | Cell Movement | Hypertension, Pulmonary - complications | Flow cytometry | CC chemokine receptors | Animal models | Antibodies | Smooth muscle | Cytotoxicity | pH effects | Blood | Metastases | CCL22 protein | CCR2 protein | Apolipoprotein E | Rodents | Bone marrow | Food | Pulmonary arteries | Bronchus | Inflammation | Ribonucleic acid--RNA | Anti-inflammatory agents | Polymerase chain reaction | Studies | Lungs | Arteriosclerosis | Hypoxia | Hemodynamics | Ventricle | Laboratory animals | Monocyte chemoattractant protein 1
Journal Article
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 05/2013, Volume 48, Issue 5, pp. 568 - 577
Journal Article
Respiratory Research, ISSN 1465-9921, 04/2017, Volume 18, Issue 1, pp. 64 - 14
Journal Article
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 09/2016, Volume 55, Issue 3, pp. 337 - 351
Excessive growth of pulmonary arterial (PA) smooth muscle cells (SMCs) is a major component of PA hypertension (PAH). The calcium-activated neutral cysteine... 
Calpain | Pulmonary hypertension | Calpastatin | GLOMERULONEPHRITIS | SYSTEM | ACTIVATION | pulmonary hypertension | BIOCHEMISTRY & MOLECULAR BIOLOGY | MUSCLE-CELL PROLIFERATION | calpastatin | M-CALPAIN | CELL BIOLOGY | calpain | INHIBITION | GENE | RESPIRATORY SYSTEM | ARTERIAL-HYPERTENSION | DISEASE | TRANSGENIC MICE | Acrylates - therapeutic use | Calpain - metabolism | Humans | Extracellular Space - drug effects | Myocytes, Smooth Muscle - pathology | Male | Promoter Regions, Genetic - genetics | Hypoxia - metabolism | Extracellular Space - metabolism | Acrylates - pharmacology | Hypertension, Pulmonary - drug therapy | Myocytes, Smooth Muscle - drug effects | Heart Function Tests | Myocytes, Smooth Muscle - metabolism | Calcium-Binding Proteins - metabolism | Cytomegalovirus - genetics | Intracellular Space - drug effects | Mice, Inbred C57BL | Mice, Transgenic | Hypertension, Pulmonary - metabolism | Hypoxia - complications | Disease Progression | Cell Movement - drug effects | Animals | Intracellular Space - metabolism | Hypoxia - physiopathology | Cell Proliferation - drug effects | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Hypertension, Pulmonary - complications | Studies | Plasma | Cytomegalovirus | Disease | Pulmonary arteries | Transgenic animals | Rodents | Sheep | Hypoxia | Kinases
Journal Article
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 09/2016, Volume 55, Issue 3, pp. 352 - 367
Journal Article
Handbook of Experimental Pharmacology, ISSN 0171-2004, 2013, Volume 218, pp. 365 - 380
The nature of the primary defect responsible for triggering and maintaining pulmonary artery smooth muscle (PA-SMC) proliferation in pulmonary artery... 
Serotonin | Smooth muscle | Pulmonary hypertension | Receptors, Serotonin - physiology | Serotonin - physiology | Serotonin Plasma Membrane Transport Proteins - physiology | Animals | Humans | Signal Transduction - physiology | Hypertension, Pulmonary - etiology
Conference Proceeding
American Journal of Physiology - Lung Cellular and Molecular Physiology, ISSN 1040-0605, 09/2012, Volume 303, Issue 6, pp. 500 - 508
Journal Article
Circulation, ISSN 0009-7322, 04/2013, Volume 127, Issue 16, pp. 1664 - 1676
Background-Induction of cellular senescence through activation of the p53 tumor suppressor protein is a new option for treating proliferative disorders.... 
ventricular remodeling | pulmonary artery | muscles | hypertension | cell aging | APOPTOSIS | CARDIAC & CARDIOVASCULAR SYSTEMS | PROLIFERATION | INHIBITION | GENE | SMOOTH-MUSCLE HYPERPLASIA | INFLAMMATION | ARTERIAL-HYPERTENSION | GROWTH | SENESCENT CELLS | MDM2 | PERIPHERAL VASCULAR DISEASE | Single-Blind Method | Tumor Suppressor Protein p53 - antagonists & inhibitors | Apoptosis - drug effects | Humans | Cellular Senescence - drug effects | Hypertension, Pulmonary - diagnostic imaging | Male | Hypertension, Pulmonary - chemically induced | Cyclin-Dependent Kinase Inhibitor p21 - deficiency | Hypertension, Pulmonary - prevention & control | Genes, p53 | Serotonin Plasma Membrane Transport Proteins - genetics | Protein Processing, Post-Translational - drug effects | Tumor Suppressor Protein p53 - agonists | Ultrasonography | Serotonin Plasma Membrane Transport Proteins - biosynthesis | Cyclin-Dependent Kinase Inhibitor p21 - physiology | Hypertension, Pulmonary - drug therapy | Imidazoles - therapeutic use | Phosphorylation - drug effects | Drug Evaluation, Preclinical | Cells, Cultured - drug effects | Serotonin Plasma Membrane Transport Proteins - physiology | Mice, Inbred C57BL | Indoles - toxicity | Mice, Transgenic | Hypoxia - complications | Imidazoles - pharmacology | Piperazines - therapeutic use | Tumor Suppressor Protein p53 - deficiency | Piperazines - pharmacology | Mice, Knockout | Pulmonary Artery - cytology | Gene Expression Regulation - drug effects | Animals | Pyrroles - toxicity | Protein Stability - drug effects | Mice | Hypertension, Pulmonary - etiology | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Endothelial Cells - drug effects | Prevention | Care and treatment | Physiological aspects | Aging | Genetic aspects | Research | Gene expression | Pulmonary hypertension | Life Sciences | Biochemistry, Molecular Biology | toxicity | cytology | remodeling | Endothelial Cells | ultrasonography | Cell Aging | Serotonin Plasma Membrane Transport Proteins | pharmacology | biosynthesis | Indoles | Anoxia | chemically induced | physiology | drug effects | agonists | Protein Processing, Post-Translational | therapeutic use | Phosphorylation | pathology | Pyrroles | Hypertension, Pulmonary | genetics | muscle | Protein Stability | drug therapy | Piperazines | complications | Cyclin-Dependent Kinase Inhibitor p21 | Cells, Cultured | Gene Expression Regulation | pulmonary | prevention & control | Pulmonary Artery | antagonists & inhibitors | etiology | Imidazoles | Tumor Suppressor Protein p53 | deficiency | Apoptosis | cell senescence
Journal Article
EUROPEAN RESPIRATORY JOURNAL, ISSN 0903-1936, 10/2019, Volume 54, Issue 4
Macrophages are major players in the pathogenesis of pulmonary arterial hypertension (PAH). To investigate whether lung macrophages and pulmonary-artery smooth... 
PATHOGENESIS | FRACTALKINE | RECRUITMENT | RESPIRATORY SYSTEM | INFLAMMATION | CCR2
Journal Article
Circulation, ISSN 0009-7322, 09/2014, Volume 130, Issue 11, pp. 880 - 891
Journal Article