Affiliation: National Institutes of Health
- Essential role of nitric oxide in acute ischemic preconditioning: S-nitros(yl)ation versus sGC/cGMP/PKG signaling?Junhui Sun
Systems Biology Center, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Free Radic Biol Med 54:105-12. 2013..In conclusion, these results suggest that the protective effect of NO is not related primarily to activation of the sGC/cGMP/PKG signaling pathway, but rather through SNO signaling in IPC-induced acute cardioprotection...
- Disruption of caveolae blocks ischemic preconditioning-mediated S-nitrosylation of mitochondrial proteinsJunhui Sun
Systems Biology Center, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Antioxid Redox Signal 16:45-56. 2012..Mitochondria are key regulators of preconditioning, and most proteins showing an increase in SNO with IPC are mitochondrial. The aim of this study was to address how IPC transduces NO/SNO signaling to mitochondria in the heart...
- Protein S-nitrosylation: a role of nitric oxide signaling in cardiac ischemic preconditioningJunhui Sun
Vascular Medicine Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Sheng Li Xue Bao 59:544-52. 2007..Thus, protein S-nitrosylation is emerging as an important contributor to cardioprotection in IPC, providing protection from cellular oxidative and nitrosative stress...
- Calcium-sensing receptor: a sensor and mediator of ischemic preconditioning in the heartJunhui Sun
Translational Medicine Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bldg 10 Rm 8N206, Bethesda, MD 20892, USA
Am J Physiol Heart Circ Physiol 299:H1309-17. 2010..Taken together, the distribution of CaSR in caveolae along with NPS2143-blockade of IPC-induced cardioprotective signaling suggest that the activation of CaSR during IPC is cardioprotective by a process involving caveolae...
- The physiological role of mitochondrial calcium revealed by mice lacking the mitochondrial calcium uniporterXin Pan
1 Center for Molecular Medicine, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA 2 National Center of Biomedical Analysis, Beijing 100850, China 3
Nat Cell Biol 15:1464-72. 2013..Taken together, these results clarify how acute alterations in mitochondrial matrix calcium can regulate mammalian physiology. ..
- Measurement of S-nitrosylation occupancy in the myocardium with cysteine-reactive tandem mass tags: short communicationMark J Kohr
Laboratory of Cardiac Physiology, Systems Biology Center, National Heart Lung and Blood Institute, Bethesda, MD 20892, USA
Circ Res 111:1308-12. 2012..However, little is known with regard to the percentage of a given protein that is modified by SNO (ie, SNO occupancy). Current methods allow for the relative quantification of SNO levels, but not for the determination of SNO occupancy...
- S-nitrosylation: a radical way to protect the heartElizabeth Murphy
Cardiac Physiology Section, Systems Biology Center, NHLBI, NIH, Bethesda, MD 20892, USA
J Mol Cell Cardiol 52:568-77. 2012..The role of nitric oxide synthase uncoupling in cardioprotection will also be addressed. This article is part of a Special Section entitled "Post-translational Modification."..
- Cyclophilin D modulates mitochondrial acetylomeTiffany Tuyen M Nguyen
From the Systems Biology Center T T M N, S M, J S, E M, Division of Cardiovascular Sciences R W, Proteomics Core Facility Y C, G W, M G, and Center for Molecular Medicine M N S, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD and Department of Pathology, Johns Hopkins Medical Center, Baltimore, MD C S
Circ Res 113:1308-19. 2013..As acetylation has been shown to regulate metabolism, we tested whether changes in protein acetylation might play a role in these metabolic changes in CypD(-/-) hearts...
- Preconditioning results in S-nitrosylation of proteins involved in regulation of mitochondrial energetics and calcium transportJunhui Sun
NHLBI, NIH, Vascular Medicine Branch, Bethesda, MD 20892, USA
Circ Res 101:1155-63. 2007..IPC and GSNO produced a similar pattern of S-nitrosylation modification and cardiac protection against ischemia/reperfusion injury, suggesting that protein S-nitrosylation may play an important cardioprotective role in heart...
- Myristoylated methionine sulfoxide reductase A protects the heart from ischemia-reperfusion injuryHang Zhao
Laboratory of Biochemistry, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 8012, USA
Am J Physiol Heart Circ Physiol 301:H1513-8. 2011..We conclude that cytosolic MsrA protects the heart from ischemia-reperfusion damage. The requirement for myristoylation suggests that MsrA must interact with a hydrophobic domain to provide protection...
- Protein S-nitrosylation and cardioprotectionJunhui Sun
Translational Medicine Branch, NHLBI, NIH, 10 Center Dr, Room 7N112, Bethesda, MD 20892, USA
Circ Res 106:285-96. 2010..A better understanding of the mechanism regulating protein S-nitrosylation and its role in cardioprotection will provide us new therapeutic opportunities and targets for interventions in cardiovascular diseases...
- Mechanism of cardioprotection: what can we learn from females?Elizabeth Murphy
NHLBI, NIH, Room 8N202, Building 10, 10 Center Drive, Bethesda, MD, USA
Pediatr Cardiol 32:354-9. 2011..It investigates estrogen signaling mediated by the nuclear estrogen receptors alpha and beta and the G-protein-coupled receptor (GPR 30/GPER). Estrogen signaling via nitric oxide and the PI3K pathway are discussed...
- S-nitrosylation: NO-related redox signaling to protect against oxidative stressJunhui Sun
National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Antioxid Redox Signal 8:1693-705. 2006..However, oxidative stress and the resultant dysfunction of NO signaling have been implicated in the pathogenesis of cardiovascular diseases...
- The NAD-dependent deacetylase SIRT2 is required for programmed necrosisNisha Narayan
Center for Molecular Medicine, National Heart, Lung and Blood Institute, NIH, Bethesda, Maryland 20892, USA
Nature 492:199-204. 2012....
- Estrogen receptor activation and cardioprotection in ischemia reperfusion injuryAnne M Deschamps
National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Trends Cardiovasc Med 20:73-8. 2010..In this review, we will focus on the signaling pathways leading to cardioprotection in ischemia reperfusion injury after ER activation and discuss the possibility and promise of specific ER modulators to treat ischemic heart diseases...
- Acute erythropoietin cardioprotection is mediated by endothelial responseRuifeng Teng
Molecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 1822, USA
Basic Res Cardiol 106:343-54. 2011..The immediate response of coronary artery endothelial cells to Epo stimulation by NO production may be a critical mechanism underlying this Epo cardioprotection...
- Deoxymyoglobin is a nitrite reductase that generates nitric oxide and regulates mitochondrial respirationSruti Shiva
Vascular Medicine Branch, Clinical Center National Institutes of Health, Bethesda, MD 20892 1662, USA
Circ Res 100:654-61. 2007....