Wei Dong Gao

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. pmc Nitroxyl-mediated disulfide bond formation between cardiac myofilament cysteines enhances contractile function
    Wei Dong Gao
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Circ Res 111:1002-11. 2012
  2. ncbi request reprint Increased cross-bridge cycling rate in stunned myocardium
    Wei Dong Gao
    Dept of Anesthesiology and Critical Care Medicine, Johns Hopkins Univ School of Medicine, Tower 711, 600 N Wolfe St, Baltimore, MD 21287, USA
    Am J Physiol Heart Circ Physiol 290:H886-93. 2006
  3. pmc Reversal of isoflurane-induced depression of myocardial contraction by nitroxyl via myofilament sensitization to Ca2+
    Wengang Ding
    Department of Anesthesiology, 2nd Affiliated Hospital, Harbin Medical University, Heilongjiang, China
    J Pharmacol Exp Ther 339:825-31. 2011
  4. pmc Nitroxyl increases force development in rat cardiac muscle
    Tieying Dai
    Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins University School of Medicine, Tower 711, 600 N Wolfe Street, Baltimore, MD 21287, USA
    J Physiol 580:951-60. 2007
  5. pmc Calcium sensitivity, force frequency relationship and cardiac troponin I: critical role of PKA and PKC phosphorylation sites
    Genaro A Ramirez-Correa
    Department of Pediatrics Division of Cardiology, Johns Hopkins University School of Medicine, Ross Bldg 1144 720 Rutland Avenue, Baltimore, MD 21205, USA
    J Mol Cell Cardiol 48:943-53. 2010
  6. doi request reprint Preservation of cardiac contractility after long-term therapy with oxypurinol in post-ischemic heart failure in mice
    Zhen Tan
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Eur J Pharmacol 621:71-7. 2009
  7. pmc Playing with cardiac "redox switches": the "HNO way" to modulate cardiac function
    Carlo G Tocchetti
    Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Antioxid Redox Signal 14:1687-98. 2011
  8. pmc Restoring redox balance enhances contractility in heart trabeculae from type 2 diabetic rats exposed to high glucose
    Niraj M Bhatt
    Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland and
    Am J Physiol Heart Circ Physiol 308:H291-302. 2015
  9. pmc Nitroxyl improves cellular heart function by directly enhancing cardiac sarcoplasmic reticulum Ca2+ cycling
    Carlo G Tocchetti
    Cardiology Division, Johns Hopkins Medical Institutions, 720 Rutland Ave, Baltimore, MD 21205, USA
    Circ Res 100:96-104. 2007
  10. pmc O-linked GlcNAc modification of cardiac myofilament proteins: a novel regulator of myocardial contractile function
    Genaro A Ramirez-Correa
    Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Circ Res 103:1354-8. 2008

Collaborators

Detail Information

Publications16

  1. pmc Nitroxyl-mediated disulfide bond formation between cardiac myofilament cysteines enhances contractile function
    Wei Dong Gao
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Circ Res 111:1002-11. 2012
    ..Nitroxyl (HNO), the one-electron-reduced form of nitric oxide, enhances cardiac function in a manner that suggests reversible cysteine modifications of the contractile machinery...
  2. ncbi request reprint Increased cross-bridge cycling rate in stunned myocardium
    Wei Dong Gao
    Dept of Anesthesiology and Critical Care Medicine, Johns Hopkins Univ School of Medicine, Tower 711, 600 N Wolfe St, Baltimore, MD 21287, USA
    Am J Physiol Heart Circ Physiol 290:H886-93. 2006
    ..Thus stunned myocardium still maintains ATP consumption in spite of lower force development, rationalizing the long-standing paradox of decreased force but unchanged oxygen consumption in the postischemic heart...
  3. pmc Reversal of isoflurane-induced depression of myocardial contraction by nitroxyl via myofilament sensitization to Ca2+
    Wengang Ding
    Department of Anesthesiology, 2nd Affiliated Hospital, Harbin Medical University, Heilongjiang, China
    J Pharmacol Exp Ther 339:825-31. 2011
    ..The present findings have potential translational value because of the efficiency and efficacy of HNO on ISO-induced myocardial contractile dysfunction...
  4. pmc Nitroxyl increases force development in rat cardiac muscle
    Tieying Dai
    Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins University School of Medicine, Tower 711, 600 N Wolfe Street, Baltimore, MD 21287, USA
    J Physiol 580:951-60. 2007
    ..This is likely to be due to modulation of myofilament proteins that harbour reactive thiolate groups that are targets of HNO...
  5. pmc Calcium sensitivity, force frequency relationship and cardiac troponin I: critical role of PKA and PKC phosphorylation sites
    Genaro A Ramirez-Correa
    Department of Pediatrics Division of Cardiology, Johns Hopkins University School of Medicine, Ross Bldg 1144 720 Rutland Avenue, Baltimore, MD 21205, USA
    J Mol Cell Cardiol 48:943-53. 2010
    ....
  6. doi request reprint Preservation of cardiac contractility after long-term therapy with oxypurinol in post-ischemic heart failure in mice
    Zhen Tan
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Eur J Pharmacol 621:71-7. 2009
    ..These results indicate that the beneficial effects of antioxidation can be sustained by long-term treatment with oxypurinol after ischemic heart failure, with significantly improved cardiac contractility...
  7. pmc Playing with cardiac "redox switches": the "HNO way" to modulate cardiac function
    Carlo G Tocchetti
    Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Antioxid Redox Signal 14:1687-98. 2011
    ....
  8. pmc Restoring redox balance enhances contractility in heart trabeculae from type 2 diabetic rats exposed to high glucose
    Niraj M Bhatt
    Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland and
    Am J Physiol Heart Circ Physiol 308:H291-302. 2015
    ..These results support the idea that maintained redox balance, via increased GSH and Trx antioxidant activities to resist oxidative stress, is an essential protective response of the diabetic heart to keep contractile function. ..
  9. pmc Nitroxyl improves cellular heart function by directly enhancing cardiac sarcoplasmic reticulum Ca2+ cycling
    Carlo G Tocchetti
    Cardiology Division, Johns Hopkins Medical Institutions, 720 Rutland Ave, Baltimore, MD 21205, USA
    Circ Res 100:96-104. 2007
    ..Rather, the data support HNO/thiolate interactions that enhance the activity of intracellular Ca(2+) cycling proteins. These findings suggest HNO donors are attractive candidates for the pharmacological treatment of heart failure...
  10. pmc O-linked GlcNAc modification of cardiac myofilament proteins: a novel regulator of myocardial contractile function
    Genaro A Ramirez-Correa
    Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Circ Res 103:1354-8. 2008
    ..This study provides the first identification of O-GlcNAcylation sites in cardiac myofilament proteins and demonstrates their potential role in regulating myocardial contractile function...
  11. pmc Apelin increases contractility in failing cardiac muscle
    Tieying Dai
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Tower 711, 600 N Wolfe Street, Baltimore, MD 21287, United States
    Eur J Pharmacol 553:222-8. 2006
    ..The increased force development is the result of increased [Ca(2+)](i) transients rather than changes in myofilament calcium responsiveness...
  12. ncbi request reprint Heart failure-associated alterations in troponin I phosphorylation impair ventricular relaxation-afterload and force-frequency responses and systolic function
    Kenneth C Bilchick
    Dept of Pediatrics, Johns Hopkins Univ School of Medicine, 720 Rutland Ave, Ross Bldg 1144, Baltimore, MD 21205, USA
    Am J Physiol Heart Circ Physiol 292:H318-25. 2007
    ..Abnormal TnI phosphorylation observed in cardiac failure may explain exacerbated relaxation delay in response to increased afterload and contribute to blunted chronotropic reserve...
  13. pmc Local control in thin filament activation of cardiac muscle
    Wei Dong Gao
    Department of Anaesthesia and Critical Care Medicine, Johns Hopkins University, Baltimore, MD 21205, USA
    J Physiol 580:358. 2007
  14. pmc Removal of Abnormal Myofilament O-GlcNAcylation Restores Ca2+ Sensitivity in Diabetic Cardiac Muscle
    Genaro A Ramirez-Correa
    Division of Cardiology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD
    Diabetes 64:3573-87. 2015
    ..Thus, preventing sarcomeric OGT and OGA displacement represents a new possible strategy for treating diabetic cardiomyopathy. ..
  15. ncbi request reprint Chronic treatment with allopurinol boosts survival and cardiac contractility in murine postischemic cardiomyopathy
    Linda B Stull
    Institute of Molecular Cardiobiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Circ Res 95:1005-11. 2004
    ..Our findings indicate that targeted blockade of just one source of oxidants, XO, impacts dramatically on the progression of postischemic cardiomyopathy in mice and prevents oxidative protein modifications...
  16. pmc Bidirectional cross-regulation between ErbB2 and β-adrenergic signalling pathways
    Polina Sysa-Shah
    Department of Molecular and Comparative Pathobiology, Johns Hopkins Medical Institutions, MRB 807, 733 N Broadway, Baltimore, MD 21205, USA
    Cardiovasc Res 109:358-73. 2016
    ..Since isoproterenol up-regulates ErbB2 in kidney and salivary glands and β2AR and ErbB2 complex in brain and heart, we hypothesized that β-adrenergic receptors (AR) modulate ErbB2 signalling status...