Xiongwen Chen

Summary

Affiliation: Temple University
Country: USA

Publications

  1. pmc β-Adrenergic stimulation increases Cav3.1 activity in cardiac myocytes through protein kinase A
    Yingxin Li
    Cardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, Pennsylvania, United States of America
    PLoS ONE 7:e39965. 2012
  2. pmc Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy
    Xiongwen Chen
    Cardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA 19140, USA
    J Mol Cell Cardiol 50:460-70. 2011
  3. pmc Reduced effects of BAY K 8644 on L-type Ca2+ current in failing human cardiac myocytes are related to abnormal adrenergic regulation
    Xiongwen Chen
    Cardiovascular Research Center and Department of Physiology, Temple University School of Medicine, 3420 North Broad Street, Philadelphia, PA 19140, USA
    Am J Physiol Heart Circ Physiol 294:H2257-67. 2008
  4. pmc Enhanced basal contractility but reduced excitation-contraction coupling efficiency and beta-adrenergic reserve of hearts with increased Cav1.2 activity
    Mingxin Tang
    Cardiovascular Research Center and Dept of Physiology, Temple Univ School of Medicine, 3400 N Broad St, Philadelphia, PA 19140, USA
    Am J Physiol Heart Circ Physiol 299:H519-28. 2010
  5. pmc Hyperphosphorylation of the cardiac ryanodine receptor at serine 2808 is not involved in cardiac dysfunction after myocardial infarction
    Hongyu Zhang
    Temple University School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 110:831-40. 2012
  6. pmc Ca2+ influx through T- and L-type Ca2+ channels have different effects on myocyte contractility and induce unique cardiac phenotypes
    Naser Jaleel
    Department of Physiology, Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA, USA
    Circ Res 103:1109-19. 2008
  7. ncbi request reprint Ca2+ influx-induced sarcoplasmic reticulum Ca2+ overload causes mitochondrial-dependent apoptosis in ventricular myocytes
    Xiongwen Chen
    Cardiovascular Research Center, Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 97:1009-17. 2005
  8. ncbi request reprint Alterations in early action potential repolarization causes localized failure of sarcoplasmic reticulum Ca2+ release
    David M Harris
    Cardiovascular Research Center, Department of Physiology, Temple University, School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 96:543-50. 2005
  9. pmc Increasing cardiac contractility after myocardial infarction exacerbates cardiac injury and pump dysfunction
    Hongyu Zhang
    Temple University, School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 107:800-9. 2010
  10. ncbi request reprint Intracellular sodium determines frequency-dependent alterations in contractility in hypertrophied feline ventricular myocytes
    Geoffrey D Mills
    Temple University School of Medicine, 3400 N Broad St, Philadelphia, PA 19140, USA
    Am J Physiol Heart Circ Physiol 292:H1129-38. 2007

Collaborators

Detail Information

Publications23

  1. pmc β-Adrenergic stimulation increases Cav3.1 activity in cardiac myocytes through protein kinase A
    Yingxin Li
    Cardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, Pennsylvania, United States of America
    PLoS ONE 7:e39965. 2012
    ..1)) in cardiomyocytes(,) which is mediated by the cAMP/PKA pathway. The upregulation of I(Ca-T(3.1)) by the β-adrenergic system could play important roles in cellular functions involving Cav3.1...
  2. pmc Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy
    Xiongwen Chen
    Cardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA 19140, USA
    J Mol Cell Cardiol 50:460-70. 2011
    ..In conclusion, increasing I(Ca-L) is sufficient to induce PCH through the calcineurin/NFAT and CaMKII/HDAC pathways. Both cytosolic and SR/ER-nuclear envelop Ca(2+) pools were shown to be involved...
  3. pmc Reduced effects of BAY K 8644 on L-type Ca2+ current in failing human cardiac myocytes are related to abnormal adrenergic regulation
    Xiongwen Chen
    Cardiovascular Research Center and Department of Physiology, Temple University School of Medicine, 3420 North Broad Street, Philadelphia, PA 19140, USA
    Am J Physiol Heart Circ Physiol 294:H2257-67. 2008
    ..Collectively, these results suggest that the decreased BAY K effects on LTCC in F HVMs are caused by increased basal channel activity, which should contribute to abnormal contractility reserve...
  4. pmc Enhanced basal contractility but reduced excitation-contraction coupling efficiency and beta-adrenergic reserve of hearts with increased Cav1.2 activity
    Mingxin Tang
    Cardiovascular Research Center and Dept of Physiology, Temple Univ School of Medicine, 3400 N Broad St, Philadelphia, PA 19140, USA
    Am J Physiol Heart Circ Physiol 299:H519-28. 2010
    ..In conclusion, increasing Cav1.2 activity by promoting its high-activity mode enhances cardiac contractility but decreases E-C coupling efficiency and the adrenergic reserve of the heart...
  5. pmc Hyperphosphorylation of the cardiac ryanodine receptor at serine 2808 is not involved in cardiac dysfunction after myocardial infarction
    Hongyu Zhang
    Temple University School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 110:831-40. 2012
    ..It has been proposed that protein kinase A (PKA) hyperphosphorylation of the RyR2 at a single residue, Ser-2808, is a critical mediator of RyR dysfunction, depressed cardiac performance, and HF after MI...
  6. pmc Ca2+ influx through T- and L-type Ca2+ channels have different effects on myocyte contractility and induce unique cardiac phenotypes
    Naser Jaleel
    Department of Physiology, Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA, USA
    Circ Res 103:1109-19. 2008
    ....
  7. ncbi request reprint Ca2+ influx-induced sarcoplasmic reticulum Ca2+ overload causes mitochondrial-dependent apoptosis in ventricular myocytes
    Xiongwen Chen
    Cardiovascular Research Center, Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 97:1009-17. 2005
    ..These results show that persistent increases in Ca2+ influx through the I(Ca-L) enhance contractility but lead to apoptosis through a mitochondrial death pathway if SR Ca2+ overload is induced...
  8. ncbi request reprint Alterations in early action potential repolarization causes localized failure of sarcoplasmic reticulum Ca2+ release
    David M Harris
    Cardiovascular Research Center, Department of Physiology, Temple University, School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 96:543-50. 2005
    ..Therefore, therapies that restore normal early repolarization should improve the contractility of the failing heart...
  9. pmc Increasing cardiac contractility after myocardial infarction exacerbates cardiac injury and pump dysfunction
    Hongyu Zhang
    Temple University, School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 107:800-9. 2010
    ..The respective roles of myocyte death and depressed myocyte contractility in the induction of HF after MI have not been clearly defined and are the focus of this study...
  10. ncbi request reprint Intracellular sodium determines frequency-dependent alterations in contractility in hypertrophied feline ventricular myocytes
    Geoffrey D Mills
    Temple University School of Medicine, 3400 N Broad St, Philadelphia, PA 19140, USA
    Am J Physiol Heart Circ Physiol 292:H1129-38. 2007
    ....
  11. pmc Cardiotoxic and cardioprotective features of chronic β-adrenergic signaling
    Xiaoying Zhang
    Cardiovascular Research Center, Department of Physiology, Temple University School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 112:498-509. 2013
    ..adrenergic signaling pathways also are capable of activating cardioprotective mechanisms...
  12. pmc CaMKII negatively regulates calcineurin-NFAT signaling in cardiac myocytes
    Scott M MacDonnell
    Department of Physiology, Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 105:316-25. 2009
    ..Cytoplasmic CaMKII regulates Ca(2+) handling proteins but whether or not it is directly involved in hypertrophic and survival signaling is not known...
  13. ncbi request reprint Adolescent feline heart contains a population of small, proliferative ventricular myocytes with immature physiological properties
    Xiongwen Chen
    Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 100:536-44. 2007
    ..Myocyte number increases during adolescent cardiac growth. These new myocytes are initially small and functionally immature, with patterns of ion channel expression normally found in the fetal/neonatal period...
  14. ncbi request reprint Calcineurin inhibition normalizes beta-adrenergic responsiveness in the spontaneously hypertensive rat
    Scott M MacDonnell
    Cardiovascular Research Center, Temple University, Philadelphia, PA, USA
    Am J Physiol Heart Circ Physiol 293:H3122-9. 2007
    ..In conclusion, CsA normalized the blunted beta-AR responsiveness associated with hypertension, in part, by mitigating calcineurin activity while improving PLB phosphorylation and subsequent sarcoplasmic reticulum Ca(2+) regulation...
  15. pmc Adrenergic regulation of cardiac contractility does not involve phosphorylation of the cardiac ryanodine receptor at serine 2808
    Scott M MacDonnell
    Department of Physiology, Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA, USA
    Circ Res 102:e65-72. 2008
    ..These results show that protein kinase A phosphorylation of ryanodine receptor Ser2808 does not have a major role in sympathetic nervous system regulation of normal cardiac function...
  16. ncbi request reprint Cellular basis of abnormal calcium transients of failing human ventricular myocytes
    Valentino Piacentino
    Molecular and Cellular Cardiology Laboratories, Cardiovascular Research Group, Temple University School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 92:651-8. 2003
    ..These changes can explain the defective Ca2+ transients of the failing human ventricular myocyte...
  17. pmc Repair of the injured adult heart involves new myocytes potentially derived from resident cardiac stem cells
    David Angert
    Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 108:1226-37. 2011
    ..The ability of the adult heart to generate new myocytes after injury is not established...
  18. pmc T-type Ca²⁺ channels regulate the exit of cardiac myocytes from the cell cycle after birth
    Fang Wang
    Cardiovascular Research Center, Temple University School of Medicine, 3500 North Broad Street, Philadelphia, PA 19140, USA
    J Mol Cell Cardiol 62:122-30. 2013
    ..The hypothesis examined in this study was the α1G TTCCs' influence in myocyte maturation and their rapid withdrawal from the cell cycle after birth...
  19. pmc GSK-3alpha directly regulates beta-adrenergic signaling and the response of the heart to hemodynamic stress in mice
    Jibin Zhou
    Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
    J Clin Invest 120:2280-91. 2010
    ..Our findings identify what we believe to be a new paradigm of regulation of beta-adrenergic signaling and raise concerns given the rapid expansion of drug development targeting GSK-3...
  20. pmc G protein-coupled receptor kinase 2 ablation in cardiac myocytes before or after myocardial infarction prevents heart failure
    Philip W Raake
    Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, 1025 Walnut St, Philadelphia, PA 19107, USA
    Circ Res 103:413-22. 2008
    ....
  21. pmc Blunted cardiac beta-adrenergic response as an early indication of cardiac dysfunction in Duchenne muscular dystrophy
    Ying Li
    Institute of Burn Research, Southwest Hospital, The Third Military Medical University, Chongqing, China Cardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA, USA
    Cardiovasc Res 103:60-71. 2014
    ..To determine whether altered beta-adrenergic responses contribute to early cardiac dysfunction in mdx (X-linked muscular dystrophy) mice, an animal model for human Duchenne muscular dystrophy...
  22. ncbi request reprint Regulated overexpression of the A1-adenosine receptor in mice results in adverse but reversible changes in cardiac morphology and function
    Hajime Funakoshi
    Center for Translational Medicine, Department of Medicine, Jefferson Medical College, Philadelphia, PA 19107, USA
    Circulation 114:2240-50. 2006
    ..To evaluate the temporal relationship between AR signaling and cardiac remodeling, we studied the effects of controlled overexpression of the A1-AR using a cardiac-specific and tetracycline-transactivating factor-regulated promoter...
  23. ncbi request reprint L-type Ca2+ channel density and regulation are altered in failing human ventricular myocytes and recover after support with mechanical assist devices
    Xiongwen Chen
    Cardiovascular Research Group, Temple University School of Medicine, Philadelphia, PA 19140, USA
    Circ Res 91:517-24. 2002
    ..These results suggest that the density of LTCC is reduced in F-HVMs but basal I(Ca,L) density is maintained by increasing in LTCC phosphorylation...

Research Grants5

  1. Ca2+-Influx Regulated Cardiac Hypertrophy, Arrhythmia and Myocyte Apoptosis
    Xiongwen Chen; Fiscal Year: 2007
    ..The Cavl.2beta2a gene will be turned on either before or after the introduction of stressors. The long-term goal is to identify new targets or strategies for treating heart disease. ..
  2. Ca2+-Influx Regulated Cardiac Hypertrophy, Arrhythmia and Myocyte Apoptosis
    Xiongwen Chen; Fiscal Year: 2009
    ..The Cavl.2beta2a gene will be turned on either before or after the introduction of stressors. The long-term goal is to identify new targets or strategies for treating heart disease. ..
  3. Ca2+-Influx Regulated Cardiac Hypertrophy, Arrhythmia and Myocyte Apoptosis
    Xiongwen Chen; Fiscal Year: 2010
    ..The Cavl.2beta2a gene will be turned on either before or after the introduction of stressors. The long-term goal is to identify new targets or strategies for treating heart disease. ..
  4. Ca2+-Influx Regulated Cardiac Hypertrophy, Arrhythmia and Myocyte Apoptosis
    Xiongwen Chen; Fiscal Year: 2009
    ..The Cavl.2beta2a gene will be turned on either before or after the introduction of stressors. The long-term goal is to identify new targets or strategies for treating heart disease. ..