PH.D. University of Gothenburg
M.Sc. Southeast University Medical College
Bachelor of Medicine Southeast University Medical College
Office: Medical Sciences Building, M254
Visit: Dr. Feng's Home Page
Visit: CIHR Group in Vascular Biology
See Publications by Qingping Feng on PubMed
Research in my laboratory is to understand pathophysiological mechanisms of heart failure and molecular regulation of fetal heart development. We utilize a wide range of approaches ranging from cellular, molecular biology to in vivo physiology and pharmacology. Current research is focused on the role of nitric oxide in fetal heart development and heart failure post myocardial infarction. We have recently demonstrated that nitric oxide is important for fetal heart development. To further understand how nitric oxide contributes to fetal heart development, we are studying the effects of nitric oxide on proliferation of fetal and neonatal cardiomyocytes. Erythropoietin, a glycoprotein essential for red blood cell production, has cardioprotective effects. Ongoing studies are investigating the role of nitric oxide in the cardioprotective effects of erythropoietin following myocardial infarction. Bone marrow stem cells have been shown to migrate to the ischemic heart and participate in cardiac repair post myocardial infarction. We are investigating factors regulating bone marrow stem cell migration to ischemic heart and the ability of the stem cells to repair the infarcted heart. Another area of our research is to study the signal transduction mechanisms in cardiomyocytes in sepsis. Sepsis causes multi-organ dysfunction including the heart. Cytokine production such as tumor necrosis factor (TNF)-alpha contributes significantly to the development of cardiac dysfunction during sepsis. Current studies are focused on signal transduction pathways by which TNF-alpha is produced in cardiomyocytes and how they contribute to cardiac dysfunction during sepsis. Genetically altered mice are employed to identify the contribution of a specific gene in the regulation of cardiovascular function in myocardial infarction, heart failure and sepsis. Studies are currently funded by Canadian Institutes of Health Research and the Heart & Stroke Foundation of Canada.
Burger D, Lu X, Lei M, Xiang F, Hammoud L, Jiang M, Wang H, Jones DL, Sims SM, Feng Q. Neuronal nitric oxide synthase protects against myocardial infarction-induced ventricular arrhythmia and mortality in mice. Circulation. 2009; 120:1345-1354.
Xiang FL, Lu X, Hammoud L, Zhu P, Robbins J, Feng Q. Cardiomyocyte specific overexpression of human stem cell factor improves cardiac function and survival post myocardial infarction in mice. Circulation. 2009; 120:1065-1074.
Li N, Lu X, Zhao X, Xiang FL, Xenocostas A, Karmazyn M, Feng Q. Endothelial nitric oxide synthase promotes mesenchymal stromal cell migration towards the ischemic myocardium through upregulation of SDF-1alpha. Stem Cells. 2009; 27:961-970.
Hammoud L, Burger D, Lu X, Feng Q. Tissue inhibitor of metalloproteinase-3 inhibits neonatal mouse cardiomyocyte proliferation via EGFR/JNK/SP-1 signaling. Am J Physiology: Cell Physiol. 2009; 296:C735-C745.
Burger D, Xiang FL, Hammoud L, Jones DL, Feng Q. Erythropoietin protects the heart from ventricular arrhythmia during ischemia and reperfusion via neuronal nitric oxide synthase. J Pharmacol Exp Ther. 2009; 329:900-907.
Burger D, Xiang F, Hammoud L, Lu X, Feng Q. Erythropoietin protects cardiomyocytes from apoptosis during myocardial ischemia and reperfusion via heme oxygenase-1. Am J Physiology: Heart and Circ Physiol. 2009; 296:H84-H93.
Peng T, Zhang T, Lu X, Feng Q. JNK1/c-fos inhibits cardiomyocyte TNF-alpha expression via a negative crosstalk with ERK and p38 MAPK in endotoxemia. Cardiovasc Res. 2009 81:733-741.
Lepic E, Burger D, Lu X, Song W, Feng Q. Lack of endothelial nitric oxide synthase decreases cardiomyocyte proliferation and delays cardiac maturation. Am J Physiol: Cell Physiol. 2006; 291:C1240-C1246.
Geoghegan-Morphet N, Burger D, Lu X, Sathish V, Peng T, Sims SM, Feng Q. Role of neuronal nitric oxide synthase in lipopolysaccharide-induced tumor necrosis factor-alpha expression in neonatal mouse cardiomyocytes. Cardiovasc Res. 2007; 75:408-416.
Lu X, Hamilton JA, Shen Ji, Jones DL, Potter RF, Arnold JMO, Feng Q. Role of tumor necrosis factor-alpha in myocardial dysfunction and apoptosis during hindlimb ischemia and reperfusion. Critical Care Medicine. 2006; 34:484-491.
Burger D, Lei M, Geoghegan-Morphet N, Lu X, Xenocostas A, Feng Q. Erythropoietin protects cardiomyocytes from apoptosis via up-regulation of endothelial nitric oxide synthase.Cardiovascular Res. 2006; 72:51-59. This paper was one of most downloaded papers in this journal in 2006 (see Cardiovascular Research 73:619-622, 2007).
Peng T, Lu X, Feng Q. Pivotal role of gp91phox-containing NADH oxidase in lipopolysaccharide-induced tumor necrosis factor-alpha expression and myocardial depression.Circulation. 2005;111:1637-1644.
Feng Q, Song W, Lu X, Hamilton J, Lei M, Peng T, Yee SP. Development of heart failure and congenital septal defects in mice lacking endothelial nitric oxide synthase. Circulation. 2002;106:873-879. This paper was featured on the cover of Circulation on Aug. 13, 2002.
Feng Q, Lu X, Jones DL, Shen J, Arnold JMO. Increased inducible nitric oxide synthase expression contributes to myocardial dysfunction and higher mortality post myocardial infarction in mice. Circulation. 2001;104:700-704.