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1. Full Text NETs Activate Pulmonary Arterial Endothelial Cells
by Rabinovitch, Marlene
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 10/2016, Volume 36, Issue 10, pp. 2035 - 2037
aneurysm | PEPTIDYLARGININE DEIMINASE INHIBITION | MITOCHONDRIAL | endothelial cell | apoptosis | chromatin | neutrophil | PATHOGENESIS | NEUTROPHIL EXTRACELLULAR TRAPS | DNA | INFLAMMATION | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | Index Medicus
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2. Full Text Autophagy proteins regulate innate immune responses by inhibiting the release of mitochondrial DNA mediated by the NALP3 inflammasome
by Nakahira, Kiichi and Fitzgerald, Katherine A and Haspel, Jeffrey Adam and Rabinovitch, Marlene and Kim, Hong Pyo and Cernadas, Manuela and Ryter, Stefan W and Dolinay, Tamas and Choi, Augustine M K and Lam, Hilaire C and Rathinam, Vijay A K and Lee, Seon-Jin and Englert, Joshua A
Nature Immunology, ISSN 1529-2908, 03/2011, Volume 12, Issue 3, pp. 222 - 230
Autophagy, a cellular process for organelle and protein turnover, regulates innate immune responses. Here we demonstrate that depletion of the autophagic... 
AIM2 INFLAMMASOME | OXIDATIVE STRESS | ACTIVATION | INTRACELLULAR DNA | DISEASE | HOST-DEFENSE | IL-1-BETA | MECHANISMS | IMMUNOLOGY | FRANCISELLA-TULARENSIS | ENDOTOXIC-SHOCK | Animals | Flow Cytometry | NLR Family, Pyrin Domain-Containing 3 Protein | Inflammasomes - immunology | DNA, Mitochondrial | Caspase 1 - immunology | Mice | Immunity, Innate | Autophagy | Carrier Proteins - immunology | Autophagy (Cytology) | Immune response | Physiological aspects | Genetic aspects | Mitochondrial DNA | Research | Macrophages | Properties | Index Medicus
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3. Full Text In Pulmonary Arterial Hypertension, Reduced BMPR2 Promotes Endothelial-to-Mesenchymal Transition via HMGA1 and Its Target Slug
by Hopper, Rachel K and Moonen, Jan-Renier A. J and Diebold, Isabel and Cao, Aiqin and Rhodes, Christopher J and Tojais, Nancy F and Hennigs, Jan K and Gu, Mingxia and Wang, Lingli and Rabinovitch, Marlene
Circulation, ISSN 0009-7322, 05/2016, Volume 133, Issue 18, pp. 1783 - 1794
Background-We previously reported high-throughput RNA sequencing analyses that identified heightened expression of the chromatin architectural factor High... 
endothelial-to-mesenchymal transition | hypertension, pulmonary | HMGA1 protein | Epithelial-Mesenchymal Transition - physiology | Humans | Middle Aged | Myocytes, Smooth Muscle - pathology | Infant | Male | Snail Family Transcription Factors - biosynthesis | Young Adult | HMGA1a Protein - biosynthesis | Snail Family Transcription Factors - genetics | Adult | Female | Child | Myocytes, Smooth Muscle - metabolism | HMGA1a Protein - genetics | Bone Morphogenetic Protein Receptors, Type II - genetics | Bone Morphogenetic Protein Receptors, Type II - deficiency | Cells, Cultured | Hypertension, Pulmonary - genetics | Mice, Transgenic | Hypertension, Pulmonary - metabolism | Animals | Endothelium, Vascular - metabolism | Adolescent | Endothelium, Vascular - pathology | Mice | Hypertension, Pulmonary - pathology | RNA sequencing | Care and treatment | Research | Pulmonary hypertension | Cell adhesion molecules | Index Medicus | Abridged Index Medicus | Endothelial-to-Mesenchymal Transition | HMGA1 | Pulmonary Hypertension
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4. Full Text Relation of Cytokine Profile to Clinical and Hemodynamic Features in Young Patients with Congenital Heart Disease and Pulmonary Hypertension
by Zorzanelli, Leína, MD and Maeda, Nair, PhD and Clavé, Mariana, BSc and Thomaz, Ana, MD and Galas, Filomena, MD and Rabinovitch, Marlene, MD and Lopes, Antonio, MD
American Journal of Cardiology, The, ISSN 0002-9149, 2016, Volume 119, Issue 1, pp. 119 - 125
Abstract In congenital heart disease, severity of pulmonary hypertension and operability are defined by noninvasive parameters (clinical history, physical... 
Cardiovascular | DEFECTS | CARDIAC & CARDIOVASCULAR SYSTEMS | INFLAMMATION | ARTERIAL-HYPERTENSION | BIOPSY | RATIO | SHUNTS | Heart Defects, Congenital - surgery | Humans | Hypertension, Pulmonary - surgery | Child, Preschool | Hypertension, Pulmonary - physiopathology | Infant | Male | Hypertension, Pulmonary - blood | Hemodynamics - physiology | Female | Heart Defects, Congenital - physiopathology | Sildenafil Citrate - administration & dosage | Vasodilator Agents - administration & dosage | Cytokines - blood | Heart Defects, Congenital - blood | Medical colleges | Genetic disorders | Interleukins | Vasodilators | Cardiac patients | Congenital heart disease | Down syndrome | T cells | Heart diseases | Pulmonary hypertension | Variables | Pediatrics | Congenital diseases | Cytokines | Rodents | Surgery | Blood pressure | Circulatory system | Intubation | Defects | Index Medicus | Abridged Index Medicus
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5. Full Text Development of pulmonary arterial hypertension in mice over-expressing S100A4/Mts1 is specific to females
by Dempsie, Yvonne and Nilsen, Margaret and White, Kevin and Mair, Kirsty M and Loughlin, Lynn and Ambartsumian, Noona and Rabinovitch, Marlene and MacLean, Margaret R
Respiratory Research, ISSN 1465-9921, 12/2011, Volume 12, Issue 1, pp. 1 - 12
Idiopathic and familial forms of pulmonary arterial hypertension (PAH) occur more frequently in women than men. However, the reason for this remains unknown.... 
Medicine & Public Health | Pneumology/Respiratory System | BREAST-CANCER | SEROTONIN TRANSPORTER | CONVERGING EVIDENCE | GENE | RESPIRATORY SYSTEM | ESTRADIOL | ESTROGEN | RATS | RECEPTOR | MONOCROTALINE | HYPOXIA | Immunohistochemistry | Up-Regulation | Cell Proliferation | Muscle, Smooth, Vascular - metabolism | Blood Pressure - genetics | S100 Calcium-Binding Protein A4 | Myocytes, Smooth Muscle - pathology | Hypertension, Pulmonary - physiopathology | Male | Pulmonary Artery - metabolism | S100 Proteins - genetics | Mice, Inbred CBA | Female | Hypertrophy, Right Ventricular - metabolism | Myocytes, Smooth Muscle - metabolism | Real-Time Polymerase Chain Reaction | Receptor for Advanced Glycation End Products | Hypertrophy, Right Ventricular - genetics | Disease Models, Animal | Estradiol - metabolism | Genetic Predisposition to Disease | Signal Transduction | Mice, Inbred C57BL | Cells, Cultured | Familial Primary Pulmonary Hypertension | Hypertension, Pulmonary - genetics | Mice, Transgenic | S100 Proteins - metabolism | Hypertension, Pulmonary - metabolism | Pulmonary Artery - physiopathology | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Muscle, Smooth, Vascular - pathology | Phenotype | Animals | Analysis of Variance | Sex Factors | Mice | Ventricular Pressure | Receptors, Immunologic - genetics | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Receptors, Immunologic - metabolism | Ventricular Function, Right | Genetic aspects | Research | Demographic aspects | Calcium-binding proteins | Pulmonary hypertension | Risk factors | Heart enlargement | Physiological aspects | Sex discrimination | Gene expression | Estradiol | Protein binding | Hypertension | Proteins | Pulmonary arteries | Rodents | Veins & arteries | Index Medicus
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6. Full Text FK506 activates BMPR2, rescues endothelial dysfunction, and reverses pulmonary hypertension
by Spiekerkoetter, Edda and Tian, Xuefei and Cai, Jie and Hopper, Rachel K and Sudheendra, Deepti and Li, Caiyun G and El-Bizri, Nesrine and Sawada, Hirofumi and Haghighat, Roxanna and Chan, Roshelle and Haghighat, Leila and De Jesus Perez, Vinicio and Wang, Lingli and Reddy, Sushma and Zhao, Mingming and Bernstein, Daniel and Solow-Cordero, David E and Beachy, Philip A and Wandless, Thomas J and Ten Dijke, Peter and Rabinovitch, Marlene
Journal of Clinical Investigation, ISSN 0021-9738, 08/2013, Volume 123, Issue 8, pp. 3600 - 3613
Dysfunctional bone morphogenetic protein receptor-2 (BMPR2) signaling is implicated in the pathogenesis of pulmonary arterial hypertension (PAH). We used a... 
MEDICINE, RESEARCH & EXPERIMENTAL | GENE | BONE MORPHOGENETIC PROTEIN | ARTERIAL-HYPERTENSION | HEART-FAILURE | IN-VIVO | APELIN | SMOOTH-MUSCLE-CELLS | TGF-BETA RECEPTOR | EXPRESSION | T-CELLS | Cell Proliferation | Humans | Microvessels - pathology | Male | Cell Hypoxia | Tacrolimus - pharmacology | Hypertension, Pulmonary - drug therapy | Endothelial Cells - physiology | Bone Morphogenetic Protein Receptors, Type II - genetics | Signal Transduction | Bone Morphogenetic Protein 4 - physiology | Endothelium, Vascular - physiopathology | Rats | Hypertension, Pulmonary - metabolism | Inhibitor of Differentiation Protein 1 - metabolism | Neointima - metabolism | Rats, Sprague-Dawley | Bone Morphogenetic Protein Receptors, Type II - metabolism | Mice, Knockout | Animals | High-Throughput Screening Assays | Neointima - drug therapy | Neointima - pathology | Tacrolimus Binding Protein 1A - metabolism | Cell Line, Tumor | Inhibitor of Differentiation Protein 1 - genetics | Endothelium, Vascular - pathology | Mice | Hypertension, Pulmonary - pathology | Smad Proteins - metabolism | Pulmonary Artery - pathology | Apoptosis | Endothelial Cells - drug effects | Hypertension | Cell receptors | Physiological aspects | Cellular signal transduction | Research | Properties | Endothelium | Proteins | Medical research | Scholarships & fellowships | Research & development--R&D | Pulmonary arteries | Rodents | Hypoxia | Ligands | Mutation | Drug dosages | Index Medicus | Abridged Index Medicus
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7. Full Text Subversion of cellular autophagosomal machinery by RNA viruses
by Jackson, William T and Giddings Jr, Thomas H and Taylor, Matthew P and Mulinyawe, Sara and Rabinovitch, Marlene and Kopito, Ron R and Kirkegaard, Karla
PLoS Biology, ISSN 1544-9173, 05/2005, Volume 3, Issue 5, pp. 0861 - 0871
Infection of human cells with poliovirus induces the proliferation of double-membraned cytoplasmic vesicles whose surfaces are used as the sites of viral RNA... 
HUMAN NEUROBLASTOMA-CELLS | LEGIONELLA-PNEUMOPHILA | POLIOVIRUS INFECTION | ULTRASTRUCTURAL CHARACTERIZATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | BIOLOGY | VIRAL REPLICATION COMPLEX | DOUBLE-MEMBRANE VESICLES | MULTIVESICULAR BODY | ENDOPLASMIC-RETICULUM | ISOLATED RAT HEPATOCYTES | MAMMALIAN-CELLS | RNA, Small Interfering - genetics | Humans | Recombinant Fusion Proteins - analysis | Molecular Sequence Data | Phagosomes - physiology | RNA Viruses - physiology | Autophagy - physiology | DNA Primers | Restriction Mapping | Freeze Fracturing | RNA Interference | Virus Replication | Poliovirus - physiology | Base Sequence | Poliovirus - pathogenicity | Index Medicus | Viruses | Cell Biology | Virology | Proteins | Microscopy | Autophagy | Machinery
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8. Full Text Bone Morphogenetic Protein 2 Induces Pulmonary Angiogenesis via Wnt-β-Catenin and Wnt-RhoA-Rac1 Pathways
by Vinicio A. de Jesus Perez and Tero-Pekka Alastalo and Jenny C. Wu and Jeffrey D. Axelrod and John P. Cooke and Manuel Amieva and Marlene Rabinovitch
The Journal of Cell Biology, ISSN 0021-9525, 1/2009, Volume 184, Issue 1, pp. 83 - 99
Mutations in bone morphogenetic protein (BMP) receptor II (BMPRII) are associated with pulmonary artery endothelial cell (PAEC) apoptosis and the loss of small... 
Angiogenesis | Cell motility | Receptors | Cell growth | Small interfering RNA | Antibodies | Pseudopodia | Mice | Gene expression regulation | Endothelial cells | SIGNAL-TRANSDUCTION | ACTIVATION | ARTERIAL-HYPERTENSION | II RECEPTOR | KINASE | PLANAR CELL POLARITY | P38 MAPK | C3H10T1/2 CELLS | BMPR-II | ENDOTHELIAL GROWTH-FACTOR | CELL BIOLOGY | Cell Proliferation | Humans | Glycogen Synthase Kinase 3 beta | rhoA GTP-Binding Protein - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Phosphoproteins - metabolism | Wnt Proteins - metabolism | Pulmonary Artery - metabolism | Hypertension - genetics | Dishevelled Proteins | Endothelial Cells - physiology | Bone Morphogenetic Protein Receptors, Type II - genetics | Signal Transduction | Endothelial Cells - metabolism | Glycogen Synthase Kinase 3 - metabolism | Bone Morphogenetic Protein 2 - physiology | beta Catenin - metabolism | Bone Morphogenetic Protein Receptors, Type II - metabolism | Hypertension - metabolism | Pulmonary Artery - cytology | Neovascularization, Physiologic - physiology | Pulmonary Artery - ultrastructure | Animals | Endothelial Cells - cytology | Smad1 Protein - metabolism | Wnt3 Protein | Bone Morphogenetic Protein Receptors, Type II - physiology | Enzyme Activation | Adaptor Proteins, Signal Transducing - metabolism | rac1 GTP-Binding Protein - metabolism | Apoptosis | Cell Movement | Index Medicus
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9. Full Text Low-dose FK506 (Tacrolimus) in end-stage pulmonary arterial hypertension
by Spiekerkoetter, Edda and Sung, Yon K and Sudheendra, Deepti and Bill, Matthew and Aldred, Micheala A and Van De Veerdonk, Mariëlle C and Noordegraaf, Anton Vonk and Long-Boyle, Janel and Dash, Rajesh and Yang, Phillip C and Lawrie, Allan and Swift, Andrew J and Rabinovitch, Marlene and Zamanian, Roham T
American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 07/2015, Volume 192, Issue 2, pp. 254 - 257
THERAPY | BMPR2 | REVEAL REGISTRY | GENE | RESPIRATORY SYSTEM | LONG-TERM SURVIVAL | MUTATIONS | MORPHOGENETIC PROTEIN-RECEPTOR | CRITICAL CARE MEDICINE | Tacrolimus - therapeutic use | Double-Blind Method | Humans | Immunosuppressive Agents - therapeutic use | Middle Aged | Adult | Female | Treatment Outcome | Hypertension, Pulmonary - drug therapy | Index Medicus | Abridged Index Medicus | Correspondence
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10. Full Text Elafin reverses pulmonary hypertension via caveolin-1-dependent bone morphogenetic protein signaling
by Nickel, Nils P and Spiekerkoetter, Edda and Gu, Mingxia and Li, Caiyun G and Li, Hai and Kaschwich, Mark and Diebold, Isabel and Hennigs, Jan K and Kim, Ki-Yoon and Miyagawa, Kazuya and Wang, Lingli and Cao, Aiqin and Sa, Silin and Jiang, Xinguo and Stockstill, Raymond W and Nicolls, Mark R and Zamanian, Roham T and Bland, Richard D and Rabinovitch, Marlene
American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 06/2015, Volume 191, Issue 11, pp. 1273 - 1286
Rationale: Pulmonary arterial hypertension is characterized by endothelial dysfunction, impaired bone morphogenetic protein receptor 2 (BMPR2) signaling, and... 
Endothelial cell apoptosis | Arterial smooth muscle cells | Neutrophil elastase inhibition | Pulmonary vascular regeneration and angiogenesis | Apelin | SURVIVAL | apelin | pulmonary vascular regeneration and angiogenesis | neutrophil elastase inhibition | endothelial cell apoptosis | arterial smooth muscle cells | RECEPTOR | PATHOGENESIS | RESPIRATORY SYSTEM | ARTERIAL-HYPERTENSION | SERINE ELASTASE INHIBITOR | SMOOTH-MUSCLE-CELLS | MICE | GROWTH-FACTOR | EXPRESSION | TENASCIN-C | CRITICAL CARE MEDICINE | Bone Morphogenetic Protein Receptors, Type II - drug effects | Apoptosis - drug effects | Humans | Pancreatic Elastase - drug effects | Cells, Cultured | Rats | Protease Inhibitors - pharmacology | Animals | Signal Transduction - drug effects | Caveolin 1 - drug effects | Hypertension, Pulmonary - drug therapy | Myocytes, Smooth Muscle - drug effects | Elafin - pharmacology | Endothelial Cells - drug effects | Index Medicus | Abridged Index Medicus | Original
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11. Full Text Autophagic protein LC3B confers resistance against hypoxia-induced pulmonary hypertension
by Lee, Seon-Jin and Smith, Akaya and Guo, Lanping and Alastalo, Tero-Pekka and Li, Molong and Sawada, Hirofumi and Liu, Xiaoli and Chen, Zhi-Hua and Ifedigbo, Emeka and Jin, Yang and Feghali-Bostwick, Carol and Ryter, Stefan W and Kim, Hong Pyo and Rabinovitch, Marlene and Choi, Augustine M. K
American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 03/2011, Volume 183, Issue 5, pp. 649 - 658
Rationale. Pulmonary hypertension (PH) is a progressive disease with unclear etiology. The significance of autophagy in PH remains unknown. Objectives: To... 
Hypertension | Hypoxia | Autophagy | Pulmonary | hypoxia | MESSENGER-RNA TRANSLATION | autophagy | MICROTUBULE-ASSOCIATED PROTEIN-1 | pulmonary | KNOCKOUT MICE | RESPIRATORY SYSTEM | ARTERIAL-HYPERTENSION | ENDOTHELIAL-CELLS | DISEASE | SMOOTH-MUSCLE-CELLS | LIGHT-CHAIN 3 | hypertension | MOLECULAR-MECHANISMS | SELF-DIGESTION | CRITICAL CARE MEDICINE | Biomarkers - metabolism | Cell Proliferation | Reactive Oxygen Species - metabolism | Microtubule-Associated Proteins - metabolism | Humans | Middle Aged | Male | Hypertension, Pulmonary - metabolism | Microscopy, Electron | Blotting, Western | Cell Hypoxia | Animals | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Lung - ultrastructure | Adult | Female | Lung - metabolism | Mice | Hypertension, Pulmonary - etiology | Index Medicus | Abridged Index Medicus | F. Pulmonary Vascular Disease | hypertension, pulmonary
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12. Full Text Prolonged mechanical ventilation with air induces apoptosis and causes failure of alveolar septation and angiogenesis in lungs of newborn mice
by Lucia M. Mokres and Kakoli Parai and Anne Hilgendorff and Robert Ertsey and Cristina M. Alvira and Marlene Rabinovitch and Richard D. Bland
American Journal of Physiology - Lung Cellular and Molecular Physiology, ISSN 1040-0605, 01/2010, Volume 298, Issue 1, pp. 23 - 35
Defective lung septation and angiogenesis, quintessential features of neonatal chronic lung disease (CLD), typically result from lengthy exposure of developing... 
Elastin | Mechanical stretch | Transforming growth factor-β | Bronchopulmonary dysplasia | Neonatal chronic lung disease | Alveolar and pulmonary capillary formation | Vascular endothelial growth factor | Lung growth and development | PHYSIOLOGY | TGF-BETA | BRONCHOPULMONARY-DYSPLASIA | PRETERM LAMBS | alveolar and pulmonary capillary formation | mechanical stretch | bronchopulmonary dysplasia | elastin | RAT LUNG | transforming growth factor-beta | EPITHELIAL-CELLS | RESPIRATORY SYSTEM | vascular endothelial growth factor | TRANSFORMING GROWTH-FACTOR-BETA-1 | neonatal chronic lung disease | NEONATAL MOUSE LUNG | SMOOTH-MUSCLE-CELLS | lung growth and development | HYALINE-MEMBRANE DISEASE | ENDOTHELIAL GROWTH-FACTOR | Cell Proliferation | Cell Count | Immunoblotting | Vascular Endothelial Growth Factor A - metabolism | Phosphoproteins - metabolism | Neovascularization, Pathologic - pathology | Time Factors | Pulmonary Alveoli - metabolism | Surface Properties | Lung - metabolism | Animals, Newborn | Elastin - metabolism | Lung - pathology | Pulmonary Alveoli - pathology | Endothelial Cells - metabolism | Smad2 Protein - metabolism | Vascular Endothelial Growth Factor Receptor-2 - metabolism | Vascular Endothelial Growth Factor Receptor-1 - metabolism | Air | Respiration, Artificial | Animals | Models, Biological | Mice | Endothelial Cells - pathology | Lung - blood supply | Transforming Growth Factor beta - metabolism | Apoptosis | Usage | Care and treatment | Lung diseases | Physiological aspects | Research | Artificial respiration | Risk factors | Studies | Immunohistochemistry | Signal transduction | Angiogenesis | Lungs | Rodents | Ventilation | Index Medicus | transforming growth factor-β
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