Wei Dong Gao
Affiliation: Johns Hopkins University
- Nitroxyl-mediated disulfide bond formation between cardiac myofilament cysteines enhances contractile functionWei 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...
- Increased cross-bridge cycling rate in stunned myocardiumWei 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...
- 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...
- Nitroxyl increases force development in rat cardiac muscleTieying 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...
- Calcium sensitivity, force frequency relationship and cardiac troponin I: critical role of PKA and PKC phosphorylation sitesGenaro 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....
- Preservation of cardiac contractility after long-term therapy with oxypurinol in post-ischemic heart failure in miceZhen 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...
- Playing with cardiac "redox switches": the "HNO way" to modulate cardiac functionCarlo G Tocchetti
Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
Antioxid Redox Signal 14:1687-98. 2011....
- Nitroxyl improves cellular heart function by directly enhancing cardiac sarcoplasmic reticulum Ca2+ cyclingCarlo 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...
- O-linked GlcNAc modification of cardiac myofilament proteins: a novel regulator of myocardial contractile functionGenaro 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...
- Apelin increases contractility in failing cardiac muscleTieying 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...
- Heart failure-associated alterations in troponin I phosphorylation impair ventricular relaxation-afterload and force-frequency responses and systolic functionKenneth 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...
- Local control in thin filament activation of cardiac muscleWei Dong Gao
Department of Anaesthesia and Critical Care Medicine, Johns Hopkins University, Baltimore, MD 21205, USA
J Physiol 580:358. 2007
- Chronic treatment with allopurinol boosts survival and cardiac contractility in murine postischemic cardiomyopathyLinda 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...