Marlene Rabinovitch

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. pmc Bone morphogenetic protein 2 induces pulmonary angiogenesis via Wnt-beta-catenin and Wnt-RhoA-Rac1 pathways
    Vinicio A de Jesus Perez
    Department of Medicine, Stanford University, Stanford, CA 94305, USA
    J Cell Biol 184:83-99. 2009
  2. pmc Inflammation and immunity in the pathogenesis of pulmonary arterial hypertension
    Marlene Rabinovitch
    From the Cardiovascular Institute and Department of Pediatrics M R and Department of Medicine M R N, Stanford University School of Medicine, CA INSERM UMR_S 999, LabEx LERMIT, Centre Chirurgical Marie Lannelongue, Le Plessis Robinson and Université Paris Sud, School of Medicine, Le Kremlin Bicêtre C G, M H and AP HP, Service de Pneumologie, Centre de référence de l hypertension pulmonaire sévère, DHU Thorax Innovation, Hopital de Bicetre, France M H
    Circ Res 115:165-75. 2014
  3. pmc Molecular pathogenesis of pulmonary arterial hypertension
    Marlene Rabinovitch
    Stanford University School of Medicine, Stanford, California 94305 5162, USA
    J Clin Invest 122:4306-13. 2012
  4. pmc Development of pulmonary arterial hypertension in mice over-expressing S100A4/Mts1 is specific to females
    Yvonne Dempsie
    College of Medical, Veterinary and Life Sciences, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK
    Respir Res 12:159. 2011
  5. ncbi request reprint Point:Counterpoint: Chronic hypoxia-induced pulmonary hypertension does/does not lead to loss of pulmonary vasculature
    Marlene Rabinovitch
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA
    J Appl Physiol 103:1449-51. 2007
  6. ncbi request reprint Pathobiology of pulmonary hypertension
    Marlene Rabinovitch
    Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305, USA
    Annu Rev Pathol 2:369-99. 2007
  7. ncbi request reprint Cellular and molecular pathobiology of pulmonary hypertension conference summary
    Marlene Rabinovitch
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305 5162, USA
    Chest 128:642S-646S. 2005
  8. pmc Molecular pathogenesis of pulmonary arterial hypertension
    Marlene Rabinovitch
    Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305 5162, USA
    J Clin Invest 118:2372-9. 2008
  9. pmc An antiproliferative BMP-2/PPARgamma/apoE axis in human and murine SMCs and its role in pulmonary hypertension
    Georg Hansmann
    Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305 5162, USA
    J Clin Invest 118:1846-57. 2008
  10. pmc S100A4 and bone morphogenetic protein-2 codependently induce vascular smooth muscle cell migration via phospho-extracellular signal-regulated kinase and chloride intracellular channel 4
    Edda Spiekerkoetter
    Department of Pediatrics, Stanford University School of Medicine, Stanford, Calif 94305 5162, USA
    Circ Res 105:639-47, 13 p following 647. 2009

Research Grants

  1. The BMP-PPARgamma Axis and Pulmonary Hypertension
    Marlene Rabinovitch; Fiscal Year: 2010
  2. Pulmonary Hypertension in Genetically Modified Mice
    Marlene Rabinovitch; Fiscal Year: 2007
  3. Pulmonary Hypertension in Genetically Modified Mice
    Marlene Rabinovitch; Fiscal Year: 2004
  4. Pulmonary Hypertension in Genetically Modified Mice
    Marlene Rabinovitch; Fiscal Year: 2005
  5. Pulmonary Hypertension in Genetically Modified Mice
    Marlene Rabinovitch; Fiscal Year: 2006
  6. The BMP-PPARgamma Axis and Pulmonary Hypertension
    Marlene Rabinovitch; Fiscal Year: 2009

Detail Information

Publications61

  1. pmc Bone morphogenetic protein 2 induces pulmonary angiogenesis via Wnt-beta-catenin and Wnt-RhoA-Rac1 pathways
    Vinicio A de Jesus Perez
    Department of Medicine, Stanford University, Stanford, CA 94305, USA
    J Cell Biol 184:83-99. 2009
    ..These findings suggest that the recruitment of both canonical and noncanonical Wnt pathways is required in BMP-2-mediated angiogenesis...
  2. pmc Inflammation and immunity in the pathogenesis of pulmonary arterial hypertension
    Marlene Rabinovitch
    From the Cardiovascular Institute and Department of Pediatrics M R and Department of Medicine M R N, Stanford University School of Medicine, CA INSERM UMR_S 999, LabEx LERMIT, Centre Chirurgical Marie Lannelongue, Le Plessis Robinson and Université Paris Sud, School of Medicine, Le Kremlin Bicêtre C G, M H and AP HP, Service de Pneumologie, Centre de référence de l hypertension pulmonaire sévère, DHU Thorax Innovation, Hopital de Bicetre, France M H
    Circ Res 115:165-75. 2014
    ..We show how genetic and metabolic abnormalities are inextricably linked to dysregulated immunity and adverse remodeling in the pulmonary arteries. ..
  3. pmc Molecular pathogenesis of pulmonary arterial hypertension
    Marlene Rabinovitch
    Stanford University School of Medicine, Stanford, California 94305 5162, USA
    J Clin Invest 122:4306-13. 2012
    ..Here, we describe emerging therapies based on preclinical studies that address these converging pathways...
  4. pmc Development of pulmonary arterial hypertension in mice over-expressing S100A4/Mts1 is specific to females
    Yvonne Dempsie
    College of Medical, Veterinary and Life Sciences, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK
    Respir Res 12:159. 2011
    ..We wished to investigate if the Mts1/RAGE pathway may play a role in the gender bias associated with PAH...
  5. ncbi request reprint Point:Counterpoint: Chronic hypoxia-induced pulmonary hypertension does/does not lead to loss of pulmonary vasculature
    Marlene Rabinovitch
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA
    J Appl Physiol 103:1449-51. 2007
  6. ncbi request reprint Pathobiology of pulmonary hypertension
    Marlene Rabinovitch
    Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305, USA
    Annu Rev Pathol 2:369-99. 2007
    ....
  7. ncbi request reprint Cellular and molecular pathobiology of pulmonary hypertension conference summary
    Marlene Rabinovitch
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305 5162, USA
    Chest 128:642S-646S. 2005
  8. pmc Molecular pathogenesis of pulmonary arterial hypertension
    Marlene Rabinovitch
    Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305 5162, USA
    J Clin Invest 118:2372-9. 2008
    ..Emerging treatments are aimed at inducing apoptosis of abnormal vascular cells that obstruct blood flow and at promoting regeneration of "lost" distal vasculature...
  9. pmc An antiproliferative BMP-2/PPARgamma/apoE axis in human and murine SMCs and its role in pulmonary hypertension
    Georg Hansmann
    Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305 5162, USA
    J Clin Invest 118:1846-57. 2008
    ..Thus, PPARgamma-mediated events could protect against PAH, and PPARgamma agonists may reverse PAH in patients with or without BMP-RII dysfunction...
  10. pmc S100A4 and bone morphogenetic protein-2 codependently induce vascular smooth muscle cell migration via phospho-extracellular signal-regulated kinase and chloride intracellular channel 4
    Edda Spiekerkoetter
    Department of Pediatrics, Stanford University School of Medicine, Stanford, Calif 94305 5162, USA
    Circ Res 105:639-47, 13 p following 647. 2009
    ..S100A4/Mts1 is implicated in motility of human pulmonary artery smooth muscle cells (hPASMCs), through an interaction with the RAGE (receptor for advanced glycation end products)...
  11. pmc Prolonged mechanical ventilation with air induces apoptosis and causes failure of alveolar septation and angiogenesis in lungs of newborn mice
    Lucia M Mokres
    Stanford Univ School of Medicine, CCSR Bldg, Rm 1225, 269 Campus Dr, Stanford, CA 94305 5162, USA
    Am J Physiol Lung Cell Mol Physiol 298:L23-35. 2010
    ....
  12. pmc SM22alpha-targeted deletion of bone morphogenetic protein receptor 1A in mice impairs cardiac and vascular development, and influences organogenesis
    Nesrine El-Bizri
    Cardiopulmonary Research Program, Vera Moulton Wall Center for Pulmonary Vascular Disease, Stanford University School of Medicine, Stanford, California, CA, USA
    Development 135:2981-91. 2008
    ..Thus, loss of Bmpr1a, by decreasing MMP2 and/or MMP9 activity, can account for vascular dilatation and persistence of brain microvessels, leading to the impaired organogenesis documented in the brain...
  13. pmc Neonatal mice genetically modified to express the elastase inhibitor elafin are protected against the adverse effects of mechanical ventilation on lung growth
    Anne Hilgendorff
    Department of Pediatrics, Stanford University, Stanford, California 94305 5162, USA
    Am J Physiol Lung Cell Mol Physiol 303:L215-27. 2012
    ..These results suggest that degradation and remodeling of lung elastin can contribute to defective lung growth in response to MV-O(2) and might be targeted therapeutically to prevent ventilator-induced neonatal lung injury...
  14. pmc Smooth muscle protein 22alpha-mediated patchy deletion of Bmpr1a impairs cardiac contractility but protects against pulmonary vascular remodeling
    Nesrine El-Bizri
    Cardiopulmonary Research Program, Vera Moulton Wall Center for Pulmonary Vascular Disease, Stanford University School of Medicine, Stanford, CA 94305, USA
    Circ Res 102:380-8. 2008
    ....
  15. pmc Neutrophil elastase is produced by pulmonary artery smooth muscle cells and is linked to neointimal lesions
    Yu Mee Kim
    Department of Pediatrics and the Wall Center for Pulmonary Vascular Disease, Stanford University School of Medicine, Stanford, California, USA
    Am J Pathol 179:1560-72. 2011
    ..Thus, PA SMC produce NE, and heightened production and activity of NE is linked to experimental and clinical pulmonary vascular disease...
  16. ncbi request reprint Mechanical ventilation with 40% oxygen reduces pulmonary expression of genes that regulate lung development and impairs alveolar septation in newborn mice
    Richard D Bland
    Department of Pediatrics, Stanford Univ School of Medicine, CCSR Bldg Rm 1225, 269 Campus Dr, Stanford, CA 94305 5162, USA
    Am J Physiol Lung Cell Mol Physiol 293:L1099-110. 2007
    ..These changes yielded lung structural defects similar to those observed in evolving CLD...
  17. pmc BMP promotes motility and represses growth of smooth muscle cells by activation of tandem Wnt pathways
    Vinicio A de Jesus Perez
    Department of Medicine, Stanford University, Stanford, CA 94305, USA
    J Cell Biol 192:171-88. 2011
    ..We speculate that, in response to injury, factors that subvert BMP-2-mediated tandem activation of Wnt-βC and Wnt-PCP pathways contribute to obliterative vascular disease in both the systemic and pulmonary circulations...
  18. pmc Disruption of PPARγ/β-catenin-mediated regulation of apelin impairs BMP-induced mouse and human pulmonary arterial EC survival
    Tero Pekka Alastalo
    Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305 5162, USA
    J Clin Invest 121:3735-46. 2011
    ..Taken together, our findings suggest that apelin could be effective in treating PAH by rescuing BMPR2 and PAEC dysfunction...
  19. pmc Inhibiting lung elastase activity enables lung growth in mechanically ventilated newborn mice
    Anne Hilgendorff
    Department of Pediatrics, Stanford University, Stanford, California 94305 5162, USA
    Am J Respir Crit Care Med 184:537-46. 2011
    ..These changes were associated with transforming growth factor (TGF)-β activation and increased apoptosis leading to defective alveolarization and lung growth arrest, as seen in neonatal chronic lung disease...
  20. ncbi request reprint Reactivation of gammaHV68 induces neointimal lesions in pulmonary arteries of S100A4/Mts1-overexpressing mice in association with degradation of elastin
    Edda Spiekerkoetter
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305 5162, USA
    Am J Physiol Lung Cell Mol Physiol 294:L276-89. 2008
    ..We therefore propose that early viral access to the vessel wall may be a critical determinant of the extent of vascular pathology following reactivation...
  21. pmc Cholinergic modulation of angiogenesis: role of the 7 nicotinic acetylcholine receptor
    Jenny C F Wu
    Department of Cardiovascular Medicine, Stanford University, Stanford, California 94305, USA
    J Cell Biochem 108:433-46. 2009
    ..Other subunits play a modulatory role. These findings may have therapeutic implications for diseases characterized by pathological angiogenesis...
  22. pmc Inhibition of transforming growth factor β worsens elastin degradation in a murine model of Kawasaki disease
    Cristina M Alvira
    Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305 5162, USA
    Am J Pathol 178:1210-20. 2011
    ..Thus, strategies to block TGF-β, used in those with Marfan syndrome, are unlikely to be beneficial and could be detrimental...
  23. ncbi request reprint Pulmonary arterial hypertension is linked to insulin resistance and reversed by peroxisome proliferator-activated receptor-gamma activation
    Georg Hansmann
    Department of Pediatrics, Division of Pediatric Cardiology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Circulation 115:1275-84. 2007
    ..We therefore hypothesized that insulin-resistant apoE-deficient (apoE-/-) mice would develop PAH that could be reversed by a peroxisome proliferator-activated receptor-gamma agonist (eg, rosiglitazone)...
  24. pmc Reduced BMPR2 expression induces GM-CSF translation and macrophage recruitment in humans and mice to exacerbate pulmonary hypertension
    Hirofumi Sawada
    The Vera Moulton Wall Center for Pulmonary Vascular Disease, 2 Department of Pediatrics, 3 Department of Surgery, 4 Department of Microbiology and Immunology, 5 Department of Medicine, and 6 Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305
    J Exp Med 211:263-80. 2014
    ..Thus, reduced BMPR2 can subvert a stress granule response, heighten GM-CSF mRNA translation, increase inflammatory cell recruitment, and exacerbate PAH. ..
  25. pmc FK506 activates BMPR2, rescues endothelial dysfunction, and reverses pulmonary hypertension
    Edda Spiekerkoetter
    The Vera Moulton Wall Center for Pulmonary Vascular Disease, Stanford University School of Medicine, Stanford, California 94305 5162, USA
    J Clin Invest 123:3600-13. 2013
    ..Our studies indicate that low-dose FK506 could be useful in the treatment of PAH. ..
  26. pmc Loss of adenomatous poliposis coli-α3 integrin interaction promotes endothelial apoptosis in mice and humans
    Vinicio A de Jesus Perez
    Department of Medicine, Stanford University, Stanford, CA, USA
    Circ Res 111:1551-64. 2012
    ..As bone morphogenetic proteins promote pulmonary angiogenesis by recruiting the Wnt/β-catenin pathway, we proposed that β-catenin activation could reduce loss and induce regeneration of small pulmonary arteries (PAs) and attenuate PH...
  27. ncbi request reprint Mts1/S100A4 stimulates human pulmonary artery smooth muscle cell migration through multiple signaling pathways
    Edda Spiekerkoetter
    Department of Pediatrics, Stanford University School of Medicine, Palo Alto, CA, USA
    Chest 128:577S. 2005
  28. ncbi request reprint Increased fibulin-5 and elastin in S100A4/Mts1 mice with pulmonary hypertension
    Sandra L Merklinger
    Department of Pediatrics, Stanford University School of Medicine, California, USA
    Circ Res 97:596-604. 2005
    ..Fibulin-5 was localized to pulmonary arteries and associated with thickened elastic laminae. This feature could underlie attenuation of pulmonary vascular changes in response to elevated pressure, as well as impaired reversibility...
  29. pmc LC3-mediated fibronectin mRNA translation induces fibrosarcoma growth by increasing connective tissue growth factor
    Lihua Ying
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Cell Sci 122:1441-51. 2009
    ..Expression profiling of soft tissue tumors revealed increased expression of both LC3 and CTGF in some locally invasive tumor types...
  30. ncbi request reprint Developmental expression of LC3alpha and beta: absence of fibronectin or autophagy phenotype in LC3beta knockout mice
    Gordon M Cann
    Department of Pediatrics, Stanford University School of Medicine, Stanford, California, USA
    Dev Dyn 237:187-95. 2008
    ..These results suggest novel compensatory mechanisms for loss of LC3beta, ensuring proper FN accumulation and autophagy during fetal and neonatal life...
  31. pmc Molecular determinants of lung development
    Edward E Morrisey
    Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA
    Ann Am Thorac Soc 10:S12-6. 2013
    ..This manuscript describes the summary of the discussion along with general recommendations to overcome the gaps in knowledge in lung developmental biology...
  32. doi request reprint PPARgamma and the pathobiology of pulmonary arterial hypertension
    Marlene Rabinovitch
    The Wall Center for Pulmonary Vascular Diseases, Stanford University School of Medicine, Stanford, CA, USA
    Adv Exp Med Biol 661:447-58. 2010
    ....
  33. ncbi request reprint Inflammation, growth factors, and pulmonary vascular remodeling
    Paul M Hassoun
    Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21287, USA
    J Am Coll Cardiol 54:S10-9. 2009
    ....
  34. ncbi request reprint Interdependent serotonin transporter and receptor pathways regulate S100A4/Mts1, a gene associated with pulmonary vascular disease
    Allan Lawrie
    Department of Pediatrics, Stanford University School of Medicine, CCSR Rm 2245B, 269 Campus Dr, Stanford, CA 93405 5162, USA
    Circ Res 97:227-35. 2005
    ..These data provide evidence for a mechanistic link between the 5-HT pathway and S100A4/Mts1 in pulmonary hypertension and explain how the 5-HT1B receptor and SERT are codependent in regulating S100A4/Mts1...
  35. pmc VEGF blockade inhibits angiogenesis and reepithelialization of endometrium
    Xiujun Fan
    Department of Obstetrics and Gynecology, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA 94305, USA
    FASEB J 22:3571-80. 2008
    ..In summary, we provide novel experimental data indicating that VEGF is essential for endometrial neoangiogenesis during postmenstrual/postpartum repair...
  36. doi request reprint Chronic effects of pulmonary artery stenosis on hemodynamic and structural development of the lungs
    Hedi Razavi
    Department of Bioengineering, Stanford University, California 94305 5444, USA
    Am J Physiol Lung Cell Mol Physiol 304:L17-28. 2013
    ..There are consequences on development of both lungs in the presence of an LPA stenosis at young age. These results suggest that early intervention may be necessary to optimize left lung growth and minimize right lung vascular pathology...
  37. ncbi request reprint Dysregulation of pulmonary elastin synthesis and assembly in preterm lambs with chronic lung disease
    Richard D Bland
    Department of Pediatrics, Stanford University School of Medicine, CCSR Bldg, Rm 1225, 269 Campus Drive, Stanford, CA 94305 5162, USA
    Am J Physiol Lung Cell Mol Physiol 292:L1370-84. 2007
    ..These changes, coupled with increased lung elastase activity measured in preterm lambs after MV for 1-3 days, likely contribute to CLD...
  38. pmc Nuclear factor-kappaB activation in neonatal mouse lung protects against lipopolysaccharide-induced inflammation
    Cristina M Alvira
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305 5162, USA
    Am J Respir Crit Care Med 175:805-15. 2007
    ..Injurious agents often cause less severe injury in neonates as compared with adults...
  39. ncbi request reprint Epidermal growth factor receptor blockade mediates smooth muscle cell apoptosis and improves survival in rats with pulmonary hypertension
    Sandra L Merklinger
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA
    Circulation 112:423-31. 2005
    ..This suggests that blockade of these downstream effectors may also induce regression of PAH...
  40. ncbi request reprint Elafin-overexpressing mice have improved cardiac function after myocardial infarction
    Kunio Ohta
    Program in Cardiovascular Research, The Hospital for Sick Children, Department of Pediatrics, University of Toronto, Canada
    Am J Physiol Heart Circ Physiol 287:H286-92. 2004
    ..05 for all comparisons). Thus serine elastase inhibition appears to suppress inflammation, cardiac dilatation, and dysfunction after myocardial infarct...
  41. ncbi request reprint Low molecular weight heparin and unfractionated heparin are both effective at accelerating pulmonary vascular maturation in neonatal rabbits
    Stacy B O'Blenes
    Division of Cardiovascular Surgery, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada
    Circulation 108:II161-6. 2003
    ..We hypothesized that unfractionated heparin (UFH) and low molecular weight heparin (LMWH), which promote angiogenesis and inhibit smooth muscle cell growth, could accelerate this process...
  42. ncbi request reprint Dexfenfluramine protects against pulmonary hypertension in rats
    Yoshihide Mitani
    Division of Cardiovascular Research Department of Laboratory Medicine and Pathobiology, The Hospital for Sick Children University of Toronto, Toronto, Ontario M5G1X8, Canada
    J Appl Physiol 93:1770-8. 2002
    ..05) despite induction of pulmonary artery elastase (P < 0.05), which we showed is critical in inducing experimental PVD. Thus it is possible that Dex is concomitantly offsetting the sequelae of elastase activity...
  43. ncbi request reprint Mechanical ventilation uncouples synthesis and assembly of elastin and increases apoptosis in lungs of newborn mice. Prelude to defective alveolar septation during lung development?
    Richard D Bland
    Am J Physiol Lung Cell Mol Physiol 294:L3-14. 2008
    ....
  44. ncbi request reprint Pulmonary arterial hypertension in congenital heart disease
    John T Granton
    Department of Medicine, University of Toronto, Division of Respirology and Critical Care Medicine Programme, University Health Network, 10 EN 220, 200 Elizabeth Street, Toronto, Ontario, Canada M5G 2C4
    Cardiol Clin 20:441-57, vii. 2002
    ..Despite differences in etiology and pathobiology, therapies that have proven successful for primary PAH may benefit this group of patients...
  45. ncbi request reprint Cellular and molecular pathobiology of pulmonary arterial hypertension
    Marc Humbert
    Service de Pneumologie et Reanimation Respiratoire, Centre des Maladies Vasculaires Pulmonaires, UPRES EA2705, Hopital Antoine Beclere, Universite Paris Sud, Clamart, France
    J Am Coll Cardiol 43:13S-24S. 2004
    ..Disordered proteolysis of the extracellular matrix is also evident in PAH. Future studies are required to find which if any of these abnormalities initiates PAH and which ones are best targeted to cure the disease...
  46. pmc S100A4/Mts1 produces murine pulmonary artery changes resembling plexogenic arteriopathy and is increased in human plexogenic arteriopathy
    Steven Greenway
    Division of Cardiovascular Research, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada
    Am J Pathol 164:253-62. 2004
    ..The relationship of increased S100A4/Mts1 to pathologically similar lesions in the transgenic mice and patients occurs despite differences in localization (endothelial versus smooth muscle cells)...
  47. ncbi request reprint The mouse through the looking glass: a new door into the pathophysiology of pulmonary hypertension
    Marlene Rabinovitch
    Circ Res 94:1001-4. 2004
  48. ncbi request reprint Overexpression of the serine elastase inhibitor elafin protects transgenic mice from hypoxic pulmonary hypertension
    Syed H E Zaidi
    Cardiovascular Research, Hospital for Sick Children, Department of Pediatrics, Toronto General Hospital, University Health Network, University of Toronto, Toronto, Ontario, Canada
    Circulation 105:516-21. 2002
    ..Increased serine elastase activity has been implicated in the vascular remodeling associated with chronic hypoxia-related pulmonary hypertension in rats...
  49. ncbi request reprint Caspases from apoptotic myocytes degrade extracellular matrix: a novel remodeling paradigm
    Kyle Northcote Cowan
    Division of Cardiovascular Research, Department of Pediatrics, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada
    FASEB J 19:1848-50. 2005
    ..Our results reveal a previously undescribed function for apoptotic cells and a novel paradigm whereby removal of cells is coordinated with degradation of excess extracellular matrix during remodeling in development and disease...
  50. ncbi request reprint Apolipoprotein D and platelet-derived growth factor-BB synergism mediates vascular smooth muscle cell migration
    Wesley C Y Leung
    Cardiovascular Research Program, Research Institute, The Hospital for Sick Children, and the Department of Pediatrics, University of Toronto, Canada
    Circ Res 95:179-86. 2004
    ..This study shows that apoD can be expressed or taken up by SMCs and can regulate their motility in response to growth factors...
  51. ncbi request reprint Temporal response and localization of integrins beta1 and beta3 in the heart after myocardial infarction: regulation by cytokines
    Mei Sun
    Heart and Stroke Richard Lewar Centre of Excellence and Division of Cardiology, University Health Network, Toronto, Ontario, M5G 2C4, Canada
    Circulation 107:1046-52. 2003
    ..Integrins are involved in structural remodeling and tissue repair. This study aimed to elucidate the role of the beta-integrins in cardiac remodeling after myocardial infarction (MI)...
  52. ncbi request reprint Fetal pulmonary artery diameters and their association with lung hypoplasia and postnatal outcome in congenital diaphragmatic hernia
    Jennifer Sokol
    Division of Neonatology, Hospital for Sick Children, Toronto, Ontario, Canada
    Am J Obstet Gynecol 186:1085-90. 2002
    ..We hypothesized that fetal branch pulmonary artery (PA) diameters indirectly reflect lung mass and are associated with postnatal outcome in cases of isolated congenital diaphragmatic hernia (CDH)...
  53. pmc Enhanced ERK-1/2 activation in mice susceptible to coxsackievirus-induced myocarditis
    Mary Anne Opavsky
    The Heart and Stroke Richard Lewar Centre of Excellence, The University of Toronto, Toronto, Ontario, Canada
    J Clin Invest 109:1561-9. 2002
    ..In contrast, significantly less ERK-1/2 activation is found in the hearts of myocarditis-resistant C57BL/6 mice. Therefore, the ERK-1/2 response to CVB3 infection may contribute to differential host susceptibility to viral myocarditis...
  54. ncbi request reprint Novel notions on newborn lung disease
    Marlene Rabinovitch
    Nat Med 8:664-6. 2002
  55. pmc Pulmonary arterial remodeling induced by a Th2 immune response
    Eleen Daley
    St Luke s Roosevelt Hospital, New York, NY 10019, USA
    J Exp Med 205:361-72. 2008
    ....
  56. ncbi request reprint Understanding and treating vein graft atherosclerosis
    Jennifer M Sarjeant
    Cardiovascular Research, Hospital for Sick Children, Toronto, ON, Canada
    Cardiovasc Pathol 11:263-71. 2002
    ..The purpose of this review is to summarize the knowledge regarding the pathophysiology of vein graft "atherosclerosis," as well as promising new treatments for this disease...
  57. ncbi request reprint Apolipoprotein D inhibits platelet-derived growth factor-BB-induced vascular smooth muscle cell proliferated by preventing translocation of phosphorylated extracellular signal regulated kinase 1/2 to the nucleus
    Jennifer M Sarjeant
    Cardiovascular Research Program, The Hospital for Sick Children, and the Department of Pediatrics, University of Toronto
    Arterioscler Thromb Vasc Biol 23:2172-7. 2003
    ..We therefore investigated whether apoD, which occurs free or associated with HDL, suppresses vascular smooth muscle cell (VSMC) proliferation, which is related to the pathobiology of disease...
  58. doi request reprint Emerging concepts and translational priorities in pulmonary arterial hypertension
    Evangelos D Michelakis
    Department of Medicine, Cardiology Division, Pulmonary Hypertension Program, University of Alberta, Edmonton, Alberta, Canada
    Circulation 118:1486-95. 2008
  59. ncbi request reprint Pulmonary arterial hypertension: future directions: report of a National Heart, Lung and Blood Institute/Office of Rare Diseases workshop
    John H Newman
    Departments of Medicine, Nashville VA Medical Center GRECC, and Vanderbilt University, Nashville, Tenn, USA
    Circulation 109:2947-52. 2004
  60. ncbi request reprint Gene transfer of prostaglandin synthase maintains patency of the newborn lamb arterial duct
    Tilman Humpl
    Department of Pediatrics, Division of Cardiology, Research Institute, University of Toronto, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
    Pediatr Res 58:976-80. 2005
    ..Western immunoblotting confirmed the presence of PGE synthase in the treatment group. Gene transfer of PGE synthase to the DA is feasible and will maintain patency for at least 1 wk...

Research Grants8

  1. The BMP-PPARgamma Axis and Pulmonary Hypertension
    Marlene Rabinovitch; Fiscal Year: 2010
    ..The proposed studies provide mechanistic links between impaired BMPRII/ia function and PAH and may encourage investigation of PPAR? agonists as a treatment option for PAH. ..
  2. Pulmonary Hypertension in Genetically Modified Mice
    Marlene Rabinovitch; Fiscal Year: 2007
    ..These studies should provide insights into the genetic basis for PVOD and information useful in developing strategies to arrest or reverse the process. ..
  3. Pulmonary Hypertension in Genetically Modified Mice
    Marlene Rabinovitch; Fiscal Year: 2004
    ..These studies should provide insights into the genetic basis for PVOD and information useful in developing strategies to arrest or reverse the process. ..
  4. Pulmonary Hypertension in Genetically Modified Mice
    Marlene Rabinovitch; Fiscal Year: 2005
    ..These studies should provide insights into the genetic basis for PVOD and information useful in developing strategies to arrest or reverse the process. ..
  5. Pulmonary Hypertension in Genetically Modified Mice
    Marlene Rabinovitch; Fiscal Year: 2006
    ..These studies should provide insights into the genetic basis for PVOD and information useful in developing strategies to arrest or reverse the process. ..
  6. The BMP-PPARgamma Axis and Pulmonary Hypertension
    Marlene Rabinovitch; Fiscal Year: 2009
    ..The proposed studies provide mechanistic links between impaired BMPRII/ia function and PAH and may encourage investigation of PPAR? agonists as a treatment option for PAH. ..