Jane A Leopold

Summary

Affiliation: Boston University School of Medicine
Country: USA

Publications

  1. ncbi request reprint Cyclic strain modulates resistance to oxidant stress by increasing G6PDH expression in smooth muscle cells
    J A Leopold
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Am J Physiol Heart Circ Physiol 279:H2477-85. 2000
  2. ncbi request reprint Glucose-6-phosphate dehydrogenase overexpression decreases endothelial cell oxidant stress and increases bioavailable nitric oxide
    Jane A Leopold
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, 700 Albany St CABR W 507, Boston, MA 02118, USA
    Arterioscler Thromb Vasc Biol 23:411-7. 2003
  3. ncbi request reprint Glucose-6-phosphate dehydrogenase modulates vascular endothelial growth factor-mediated angiogenesis
    Jane A Leopold
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Biol Chem 278:32100-6. 2003
  4. pmc Increasing glucose 6-phosphate dehydrogenase activity restores redox balance in vascular endothelial cells exposed to high glucose
    Zhaoyun Zhang
    Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA
    PLoS ONE 7:e49128. 2012
  5. ncbi request reprint Increased myocardial dysfunction after ischemia-reperfusion in mice lacking glucose-6-phosphate dehydrogenase
    Mohit Jain
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass 02118, USA
    Circulation 109:898-903. 2004
  6. pmc Glutathione peroxidase-3 deficiency promotes platelet-dependent thrombosis in vivo
    Richard C Jin
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Circulation 123:1963-73. 2011
  7. pmc Aldosterone increases oxidant stress to impair guanylyl cyclase activity by cysteinyl thiol oxidation in vascular smooth muscle cells
    Bradley A Maron
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 284:7665-72. 2009
  8. pmc Aldosterone inactivates the endothelin-B receptor via a cysteinyl thiol redox switch to decrease pulmonary endothelial nitric oxide levels and modulate pulmonary arterial hypertension
    Bradley A Maron
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, 75 Francis St, PBB 1, Boston, MA 02115, USA
    Circulation 126:963-74. 2012
  9. pmc Glutathione peroxidase-1 modulates lipopolysaccharide-induced adhesion molecule expression in endothelial cells by altering CD14 expression
    Edith Lubos
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, 77 Ave Louis Pasteur, Boston, MA 02115, USA
    FASEB J 24:2525-32. 2010
  10. pmc Glucose-6-phosphate dehydrogenase-deficient mice have increased renal oxidative stress and increased albuminuria
    Yizhen Xu
    Renal Division, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA
    FASEB J 24:609-16. 2010

Collaborators

Detail Information

Publications38

  1. ncbi request reprint Cyclic strain modulates resistance to oxidant stress by increasing G6PDH expression in smooth muscle cells
    J A Leopold
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Am J Physiol Heart Circ Physiol 279:H2477-85. 2000
    ..When G6PDH is inhibited, GSH levels are not restored because of impaired glutathione reductase activity. These data suggest that G6PDH is a critical determinant of the response to oxidant stress in VSMC...
  2. ncbi request reprint Glucose-6-phosphate dehydrogenase overexpression decreases endothelial cell oxidant stress and increases bioavailable nitric oxide
    Jane A Leopold
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, 700 Albany St CABR W 507, Boston, MA 02118, USA
    Arterioscler Thromb Vasc Biol 23:411-7. 2003
    ..Therefore, we examined whether overexpression of G6PD would decrease reactive oxygen species accumulation and increase bioavailable NO. in endothelial cells...
  3. ncbi request reprint Glucose-6-phosphate dehydrogenase modulates vascular endothelial growth factor-mediated angiogenesis
    Jane A Leopold
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Biol Chem 278:32100-6. 2003
    ..These findings demonstrate that G6PD modulates angiogenesis and may represent a novel angiogenic regulator...
  4. pmc Increasing glucose 6-phosphate dehydrogenase activity restores redox balance in vascular endothelial cells exposed to high glucose
    Zhaoyun Zhang
    Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA
    PLoS ONE 7:e49128. 2012
    ..These studies illustrate that increasing G6PD activity restores redox balance in endothelial cells exposed to high glucose, which is a potentially important therapeutic target to protect ECs from the deleterious effects of high glucose...
  5. ncbi request reprint Increased myocardial dysfunction after ischemia-reperfusion in mice lacking glucose-6-phosphate dehydrogenase
    Mohit Jain
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass 02118, USA
    Circulation 109:898-903. 2004
    ..We therefore hypothesized that G6PD is essential for maintaining GSH levels and protecting the heart during ischemia-reperfusion injury...
  6. pmc Glutathione peroxidase-3 deficiency promotes platelet-dependent thrombosis in vivo
    Richard C Jin
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Circulation 123:1963-73. 2011
    ..A deficiency of this enzyme has been associated with platelet-dependent thrombosis, and a promoter haplotype with reduced function has been associated with stroke risk...
  7. pmc Aldosterone increases oxidant stress to impair guanylyl cyclase activity by cysteinyl thiol oxidation in vascular smooth muscle cells
    Bradley A Maron
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 284:7665-72. 2009
    ..These findings demonstrate that pathophysiologically relevant concentrations of aldosterone increase oxidant stress to convert GC to an NO(.)-insensitive state, resulting in disruption of normal vasodilatory signaling pathways in VSMC...
  8. pmc Aldosterone inactivates the endothelin-B receptor via a cysteinyl thiol redox switch to decrease pulmonary endothelial nitric oxide levels and modulate pulmonary arterial hypertension
    Bradley A Maron
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, 75 Francis St, PBB 1, Boston, MA 02115, USA
    Circulation 126:963-74. 2012
    ..We hypothesized that aldosterone modulates PAH by disrupting ET(B)-eNOS signaling through a mechanism involving increased pulmonary endothelial oxidant stress...
  9. pmc Glutathione peroxidase-1 modulates lipopolysaccharide-induced adhesion molecule expression in endothelial cells by altering CD14 expression
    Edith Lubos
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, 77 Ave Louis Pasteur, Boston, MA 02115, USA
    FASEB J 24:2525-32. 2010
    ..Taken together, these data suggest that GPx-1 modulates the endothelial cell response to LPS, in part, by altering CD14-mediated effects...
  10. pmc Glucose-6-phosphate dehydrogenase-deficient mice have increased renal oxidative stress and increased albuminuria
    Yizhen Xu
    Renal Division, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA
    FASEB J 24:609-16. 2010
    ..These results show that decreased G6PD activity per se is sufficient to cause changes similar to those seen in diabetic mice...
  11. ncbi request reprint Glucose-6-phosphate dehydrogenase deficiency decreases vascular superoxide and atherosclerotic lesions in apolipoprotein E(-/-) mice
    Reiko Matsui
    Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA
    Arterioscler Thromb Vasc Biol 26:910-6. 2006
    ..The purpose of this study was to examine whether G6PD deficiency affects vascular oxidants and atherosclerosis in high-fat fed apolipoprotein (apo) E(-/-) mice...
  12. pmc High glucose inhibits glucose-6-phosphate dehydrogenase, leading to increased oxidative stress and beta-cell apoptosis
    Zhaoyun Zhang
    Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    FASEB J 24:1497-505. 2010
    ..G6PD plays an important role in beta-cell function and survival. High-glucose-mediated decrease in G6PD activity may provide a mechanistic explanation for the gradual loss of beta cells in patients with diabetes...
  13. pmc Glutathione peroxidase-1 deficiency augments proinflammatory cytokine-induced redox signaling and human endothelial cell activation
    Edith Lubos
    Department of Medicine, Cardiovascular Division, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 286:35407-17. 2011
    ..Targeted DUSP4 knockdown enhanced TNF-α-mediated ERK1/2 pathway activation and resulted in increased adhesion molecule expression, indicating that GPx-1 deficiency may augment TNF-α-mediated events, in part, by regulating DUSP4...
  14. pmc Aldosterone impairs vascular reactivity by decreasing glucose-6-phosphate dehydrogenase activity
    Jane A Leopold
    Whitaker Cardiovascular Institute, 700 Albany Street, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Nat Med 13:189-97. 2007
    ..These findings demonstrate that aldosterone induces a G6PD-deficient phenotype to impair endothelial function; aldosterone antagonism or gene transfer of G6pd improves vascular reactivity by restoring G6PD activity...
  15. pmc Impaired angiogenesis in glutathione peroxidase-1-deficient mice is associated with endothelial progenitor cell dysfunction
    Gennaro Galasso
    Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Circ Res 98:254-61. 2006
    ..These data suggest that EPC dysfunction is a mechanism by which elevated levels of ROS can contribute to vascular disease...
  16. pmc Bone morphogenetic protein-2 activates NADPH oxidase to increase endoplasmic reticulum stress and human coronary artery smooth muscle cell calcification
    Marcel Liberman
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Biochem Biophys Res Commun 413:436-41. 2011
    ..Thus, in HCSMC, BMP-2 increases oxidant stress and ER stress to increase Runx2 expression and promote vascular smooth muscle cell calcification...
  17. ncbi request reprint Glucose-6 phosphate dehydrogenase deficiency decreases the vascular response to angiotensin II
    Reiko Matsui
    Vascular Biology Unit, Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass 02118 2393, USA
    Circulation 112:257-63. 2005
    ..We determined the hypertensive and vascular hypertrophic response to Ang II in G6PD-deficient mice...
  18. ncbi request reprint Hypoxia potentiates nitric oxide-mediated apoptosis in endothelial cells via peroxynitrite-induced activation of mitochondria-dependent and -independent pathways
    Geoffrey A Walford
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Biol Chem 279:4425-32. 2004
    ..These findings confirm that high flux of NO* under hypoxic conditions promotes cell death via mitochondrial damage and mitochondrial-independent mechanisms by peroxynitrite...
  19. pmc Glutathione peroxidase-1 regulates mitochondrial function to modulate redox-dependent cellular responses
    Diane E Handy
    Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 284:11913-21. 2009
    ..Taken together, these data suggest that GPx-1 can modulate redox-dependent cellular responses by regulating mitochondrial function...
  20. pmc Plasma aldosterone levels are elevated in patients with pulmonary arterial hypertension in the absence of left ventricular heart failure: a pilot study
    Bradley A Maron
    Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Eur J Heart Fail 15:277-83. 2013
    ..Thus, the central aim of the current study is to determine if hyperaldosteronism is an unrecognized component of the PAH clinical syndrome...
  21. pmc Redox Pioneer: Professor Joseph Loscalzo
    Jane A Leopold
    Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Antioxid Redox Signal 13:1125-32. 2010
    ..He has received numerous awards and honors for his scientific contributions, including election to the Institute of Medicine of the National Academy of Sciences...
  22. pmc Oxidative risk for atherothrombotic cardiovascular disease
    Jane A Leopold
    Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Free Radic Biol Med 47:1673-706. 2009
    ....
  23. pmc Mineralocorticoid receptor antagonists and endothelial function
    Bradley A Maron
    Harvard Medical School, Brigham and Women s Hospital, Department of Medicine, Cardiovascular Division, 77 Avenue Louis Pasteur, NRB 0630K, Boston, MA 02115, USA
    Curr Opin Investig Drugs 9:963-9. 2008
    ..Therefore, the development of newer agents with more favorable side-effect profiles is needed...
  24. pmc Tumor necrosis factor-α-mediated suppression of dual-specificity phosphatase 4: crosstalk between NFκB and MAPK regulates endothelial cell survival
    Derrick D Kao
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, HMS NRB 0630, 77 Avenue Louis Pasteur, Boston, MA, 02115, USA
    Mol Cell Biochem 382:153-62. 2013
    ..Taken together, our findings show that DUSP4 attenuates ERK signaling and reduces cell viability, suggesting that the novel crosstalk between NFκB and MAPK pathways contributes to cell survival. ..
  25. doi request reprint Effectiveness of Spironolactone Plus Ambrisentan for Treatment of Pulmonary Arterial Hypertension (from the [ARIES] Study 1 and 2 Trials)
    Bradley A Maron
    Veterans Affairs Boston Healthcare System, Department of Cardiology, 1400 VFW, Parkway, Boston, Massachusetts Department of Internal Medicine, Division of Cardiovascular Medicine, Brigham and Women s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts Electronic address
    Am J Cardiol 112:720-5. 2013
    ..In conclusion, these pilot data suggest that coupling spironolactone and endothelin type-A receptor antagonism may be clinically beneficial in PAH. Prospective clinical trials are required to further characterize our findings. ..
  26. pmc Bone morphogenetic protein-2 decreases microRNA-30b and microRNA-30c to promote vascular smooth muscle cell calcification
    Joshua A F Balderman
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Am Heart Assoc 1:e003905. 2012
    ..One possible mechanism by which Runx2 protein expression is induced is downregulation of inhibitory microRNAs (miR)...
  27. doi request reprint Balancing role of nitric oxide in complement-mediated activation of platelets from mCd59a and mCd59b double-knockout mice
    Xuebin Qin
    Department of Medicine, Brigham and Women s Hospital, Boston, Massachusetts, USA
    Am J Hematol 84:221-7. 2009
    ..These results indicate that the thrombotic diathesis of PNH patients could be due to a combination of increased complement-mediated platelet activation and reduced NO-bioavailability as a consequence of hemolysis...
  28. ncbi request reprint Cardiogenic shock caused by right ventricular infarction: a report from the SHOCK registry
    Alice K Jacobs
    Department of Medicine, Boston Medical Center, Massachusetts 02118, USA
    J Am Coll Cardiol 41:1273-9. 2003
    ..The purpose of this study was to determine the characteristics and outcomes of patients with acute myocardial infarction (MI) complicated by cardiogenic shock due to predominant right ventricular (RV) infarction...
  29. pmc Reciprocal regulation of 11β-hydroxysteroid dehydrogenase 1 and glucocorticoid receptor expression by dexamethasone inhibits human coronary artery smooth muscle cell proliferation in vitro
    George Michas
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur, NRB 0630 K, Boston, MA 02115, USA
    Mol Cell Biochem 346:69-79. 2011
    ..These findings suggest that 11β-HSD1 plays a role in the effects of glucocorticoids on vascular smooth muscle cell phenotype...
  30. ncbi request reprint Oxidative enzymopathies and vascular disease
    Jane A Leopold
    Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass 02118, USA
    Arterioscler Thromb Vasc Biol 25:1332-40. 2005
    ..Individually, each of these polymorphisms imposes a state of uncompensated oxidant stress on the vasculature and collectively comprise the oxidative enzymopathies...
  31. ncbi request reprint Glucose-6-phosphate dehydrogenase modulates cytosolic redox status and contractile phenotype in adult cardiomyocytes
    Mohit Jain
    Cardiac Muscle Research Laboratory, Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass, USA
    Circ Res 93:e9-16. 2003
    ..The full text of this article is available online at http://www.circresaha.org...
  32. ncbi request reprint Vascular calcification: pathobiological mechanisms and clinical implications
    Rebecca C Johnson
    Cardiovascular Division, Department of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Circ Res 99:1044-59. 2006
    ..Through greater understanding of both the mechanism and clinical consequences of vascular calcification, future therapeutic strategies may be more effectively designed and applied...
  33. ncbi request reprint Atherothrombosis: plaque instability and thrombogenesis
    Frederick L Ruberg
    Evans Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118 2526, USA
    Prog Cardiovasc Dis 44:381-94. 2002
    ..Accordingly, pharmacological interventions for the treatment of ACS are directed against the initiation and propagation of thrombosis, as well as toward improvement of endothelial function...
  34. pmc Human alpha B-crystallin mutation causes oxido-reductive stress and protein aggregation cardiomyopathy in mice
    Namakkal S Rajasekaran
    Center for Cardiovascular Translational Biomedicine, Division of Cardiology, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, UT 84132, USA
    Cell 130:427-39. 2007
    ..These findings demonstrate that dysregulation of G6PD activity is necessary and sufficient for maladaptive reductive stress and suggest a novel therapeutic target for abrogating R120GCryAB cardiomyopathy and heart failure in humans...
  35. ncbi request reprint Xanthine oxidase inhibition and heart failure: novel therapeutic strategy for ventricular dysfunction?
    Roger J Hajjar
    Circ Res 98:169-71. 2006
  36. ncbi request reprint Vasoactive substances: nitric oxide and endothelial dysfunction in atherosclerosis
    Guilia Russo
    University of Padua, Padua, Italy
    Vascul Pharmacol 38:259-69. 2002
    ..Strategies to replenish bioavailable NO include the administration of organic nitrosovasodilators or NO donor compounds, therapies to improve NO synthase function, and gene therapy...
  37. ncbi request reprint Does thrombolytic therapy facilitate or foil primary PCI?
    Jane A Leopold
    N Engl J Med 358:2277-9. 2008
  38. ncbi request reprint Small-molecule glycoprotein IIb/IIIa antagonists and bleeding risk in women: too much of a good thing?
    Jane A Leopold
    Circulation 114:1344-6. 2006