Gerald W Dorn

Summary

Affiliation: University of Cincinnati
Country: USA

Publications

  1. ncbi Increased particulate partitioning of PKC epsilon reverses susceptibility of phospholamban knockout hearts to ischemic injury
    Kimberly N Gregory
    Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267 0575, USA
    J Mol Cell Cardiol 36:313-8. 2004
  2. ncbi Intracellular transport mechanisms of signal transducers
    Gerald W Dorn
    Department of Medicine, University of Cincinnati, Cincinnati, Ohio 45267 0542, USA
    Annu Rev Physiol 64:407-29. 2002
  3. ncbi The fuzzy logic of physiological cardiac hypertrophy
    Gerald W Dorn
    Center for Molecular Cardiovascular Research, University of Cincinnati, Ohio 45267-0839, USA
    Hypertension 49:962-70. 2007
  4. ncbi Myocardial angiogenesis: its absence makes the growing heart founder
    Gerald W Dorn
    Center for Molecular Cardiovascular Research, University of Cincinnati, Cincinnati, OH 45267 0839, USA
    Cell Metab 5:326-7. 2007
  5. ncbi Protein kinase cascades in the regulation of cardiac hypertrophy
    Gerald W Dorn
    Heart and Vascular Center, Medical Center, University of Cincinnati, Cincinnati, Ohio 45267 0542, USA
    J Clin Invest 115:527-37. 2005
  6. ncbi The Gordon Wilson Lecture: neurohormonal signaling pathways that link cardiac growth and death
    Gerald W Dorn
    Center for Molecular Cardiovascular Research, University of Cincinnati, Cincinnati, Ohio, USA
    Trans Am Clin Climatol Assoc 118:137-52. 2007
  7. ncbi Genetic factors in cardiac hypertrophy
    Gerald W Dorn
    Heart and Vascular Center, University of Cincinnati Medical Center, OH 45267 0542, USA
    Ann N Y Acad Sci 1015:225-37. 2004
  8. ncbi A mutation in the human phospholamban gene, deleting arginine 14, results in lethal, hereditary cardiomyopathy
    Kobra Haghighi
    Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    Proc Natl Acad Sci U S A 103:1388-93. 2006
  9. ncbi Sarcoplasmic reticulum calcium overloading in junctin deficiency enhances cardiac contractility but increases ventricular automaticity
    Qunying Yuan
    Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, OH 45267 0575, USA
    Circulation 115:300-9. 2007
  10. ncbi Cardiomyocyte degeneration with calpain deficiency reveals a critical role in protein homeostasis
    Anita S Galvez
    Center for Molecular Cardiovascular Research, University of Cincinnati, OH, USA
    Circ Res 100:1071-8. 2007

Research Grants

  1. G-Protein Receptor Kinases in Cardiac Stress Adaptation
    GERALD DORN; Fiscal Year: 2007
  2. Calpains as Mediators of Cardiac Ischemic Injury
    GERALD DORN; Fiscal Year: 2007
  3. Core--Clinical Research Skills Development
    GERALD DORN; Fiscal Year: 2007

Collaborators

Detail Information

Publications76

  1. ncbi Increased particulate partitioning of PKC epsilon reverses susceptibility of phospholamban knockout hearts to ischemic injury
    Kimberly N Gregory
    Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267 0575, USA
    J Mol Cell Cardiol 36:313-8. 2004
    ....
  2. ncbi Intracellular transport mechanisms of signal transducers
    Gerald W Dorn
    Department of Medicine, University of Cincinnati, Cincinnati, Ohio 45267 0542, USA
    Annu Rev Physiol 64:407-29. 2002
    ..The pathophysiological significance of disrupted subcellular protein transport in cell signaling and the potential therapeutic utility of targeted regulation of these events are in the process of being characterized...
  3. ncbi The fuzzy logic of physiological cardiac hypertrophy
    Gerald W Dorn
    Center for Molecular Cardiovascular Research, University of Cincinnati, Ohio 45267-0839, USA
    Hypertension 49:962-70. 2007
  4. ncbi Myocardial angiogenesis: its absence makes the growing heart founder
    Gerald W Dorn
    Center for Molecular Cardiovascular Research, University of Cincinnati, Cincinnati, OH 45267 0839, USA
    Cell Metab 5:326-7. 2007
    ..2007) describe how p53 expression in hypertrophying heart muscle impairs HIF-1-mediated neovascularization and contributes to functional decompensation of pressure-overload cardiac hypertrophy...
  5. ncbi Protein kinase cascades in the regulation of cardiac hypertrophy
    Gerald W Dorn
    Heart and Vascular Center, Medical Center, University of Cincinnati, Cincinnati, Ohio 45267 0542, USA
    J Clin Invest 115:527-37. 2005
    ..Here we review recent developments in the area of these cardiotrophic kinases, highlighting the utility of animal models that are helping to identify molecular targets in the human condition...
  6. ncbi The Gordon Wilson Lecture: neurohormonal signaling pathways that link cardiac growth and death
    Gerald W Dorn
    Center for Molecular Cardiovascular Research, University of Cincinnati, Cincinnati, Ohio, USA
    Trans Am Clin Climatol Assoc 118:137-52. 2007
    ....
  7. ncbi Genetic factors in cardiac hypertrophy
    Gerald W Dorn
    Heart and Vascular Center, University of Cincinnati Medical Center, OH 45267 0542, USA
    Ann N Y Acad Sci 1015:225-37. 2004
    ..This article reviews the role of G alpha q in the development of pressure overload hypertrophy and discusses the relationships between G alpha q and beta-adrenergic receptors, RGS proteins, and the proapoptotic factor, Nix/Bnip3L...
  8. ncbi A mutation in the human phospholamban gene, deleting arginine 14, results in lethal, hereditary cardiomyopathy
    Kobra Haghighi
    Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    Proc Natl Acad Sci U S A 103:1388-93. 2006
    ..Thus, by chronic suppression of sarcoplasmic reticulum Ca(2+)-ATPase activity, the nonreversible superinhibitory function of mutant PLN-R14Del may lead to inherited dilated cardiomyopathy and premature death in both humans and mice...
  9. ncbi Sarcoplasmic reticulum calcium overloading in junctin deficiency enhances cardiac contractility but increases ventricular automaticity
    Qunying Yuan
    Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, OH 45267 0575, USA
    Circulation 115:300-9. 2007
    ..The essential physiological effects of junctin and its potential regulatory roles in sarcoplasmic reticulum Ca cycling and Ca-dependent cardiac functions, such as myocyte contractility and automaticity, are unknown...
  10. ncbi Cardiomyocyte degeneration with calpain deficiency reveals a critical role in protein homeostasis
    Anita S Galvez
    Center for Molecular Cardiovascular Research, University of Cincinnati, OH, USA
    Circ Res 100:1071-8. 2007
    ....
  11. ncbi A human polymorphism of protein phosphatase-1 inhibitor-1 is associated with attenuated contractile response of cardiomyocytes to beta-adrenergic stimulation
    Guoli Chen
    Department of Pharmacology and Cell Biophysics, University of Cincinnati, College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267 0575, USA
    FASEB J 22:1790-6. 2008
    ..These findings suggest that the human G147D PPI-1 can attenuate responses of cardiomyocytes to beta-adrenergic agonists by decreasing PLN phosphorylation and therefore may contribute to deteriorated function in heart failure...
  12. ncbi Protein kinase Calpha negatively regulates systolic and diastolic function in pathological hypertrophy
    Harvey S Hahn
    Department of Internal Medicine, University of Cincinnati Medical Center, 231 Albert B Sabin Way, Cincinnati, Ohio 45267 0542, USA
    Circ Res 93:1111-9. 2003
    ..These results define pathological roles for PKCalpha as a negative regulator of ventricular systolic and diastolic function...
  13. ncbi Nix-mediated apoptosis links myocardial fibrosis, cardiac remodeling, and hypertrophy decompensation
    Abhinav Diwan
    Center for Molecular Cardiovascular Research, University of Cincinnati, Cincinnati, OH 45267 0839, USA
    Circulation 117:396-404. 2008
    ..Although modulation of apoptosis-regulating genes occurs in cardiac hypertrophy, a causal role for programmed cardiomyocyte death in left ventricular (LV) remodeling has not been established...
  14. ncbi Dual autonomous mitochondrial cell death pathways are activated by Nix/BNip3L and induce cardiomyopathy
    Yun Chen
    Department of Medicine, Center for Pharmacogenomics, and Departments of Medicine and Pathology and Immunology, Division of Molecular Oncology, Washington University School of Medicine, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 107:9035-42. 2010
    ..Complete protection against programmed cell death mediated by Nix and related factors can be achieved by simultaneous inhibition of both pathways...
  15. ncbi A human phospholamban promoter polymorphism in dilated cardiomyopathy alters transcriptional regulation by glucocorticoids
    Kobra Haghighi
    Department of Pharmacology and Cell Biophysics, University of Cincinnati, College of Medicine, Cincinnati, Ohio 45267 0575, USA
    Hum Mutat 29:640-7. 2008
    ..These findings suggest that the g.203A>C genetic variant in the human PLN promoter may contribute to depressed contractility and accelerate functional deterioration in heart failure...
  16. ncbi Genetic manipulation of periostin expression reveals a role in cardiac hypertrophy and ventricular remodeling
    Toru Oka
    Department of Pediatrics, University of Cincinnati, Division of Molecular Cardiovascular Biology, Children s Hospital Medical Center, Cincinnati, OH 45229 3039, USA
    Circ Res 101:313-21. 2007
    ..These are the first genetic data detailing the function of Pn in the adult heart as a regulator of cardiac remodeling and hypertrophy...
  17. ncbi MicroRNA-133a protects against myocardial fibrosis and modulates electrical repolarization without affecting hypertrophy in pressure-overloaded adult hearts
    Scot J Matkovich
    Center for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA
    Circ Res 106:166-75. 2010
    ..Because miR-133a levels decrease during reactive cardiac hypertrophy, some have considered that restoring miR-133a levels could suppress hypertrophic remodeling...
  18. ncbi Targeting erythroblast-specific apoptosis in experimental anemia
    Abhinav Diwan
    Center for Molecular Cardiovascular Research, University of Cincinnati, Cincinnati, OH, USA
    Apoptosis 13:1022-30. 2008
    ..These results support the concept of targeting erythroblast apoptosis to maximize erythrocyte production in acute anemia, which may be of value in erythropoietin resistance...
  19. ncbi Pharmacological- and gene therapy-based inhibition of protein kinase Calpha/beta enhances cardiac contractility and attenuates heart failure
    Michael Hambleton
    Department of Pediatrics, University of Cincinnati, Cincinnati Children s Hospital Medical Center, Cincinnati, Ohio 45229 3039, USA
    Circulation 114:574-82. 2006
    ....
  20. ncbi Inhibition of ischemic cardiomyocyte apoptosis through targeted ablation of Bnip3 restrains postinfarction remodeling in mice
    Abhinav Diwan
    Center for Molecular Cardiovascular Research and Department of Pediatrics, University of Cincinnati, Cincinnati, Ohio, USA
    J Clin Invest 117:2825-33. 2007
    ..These studies identify postischemic apoptosis by myocardial Bnip3 as a major determinant of ventricular remodeling in the infarcted heart, suggesting that Bnip3 may be an attractive therapeutic target...
  21. ncbi Human mutation in the anti-apoptotic heat shock protein 20 abrogates its cardioprotective effects
    Persoulla Nicolaou
    Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267 0575, USA
    J Biol Chem 283:33465-71. 2008
    ....
  22. ncbi Targeting cyclophilin D and the mitochondrial permeability transition enhances beta-cell survival and prevents diabetes in Pdx1 deficiency
    Kei Fujimoto
    Division of Endocrinology, Metabolism and Lipid Research, and Center for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 107:10214-9. 2010
    ..Thus, cyclophilin D and the mitochondrial permeability transition are critical regulators of beta-cell death caused by Pdx1 insufficiency...
  23. ncbi Receptor-independent protein kinase C alpha (PKCalpha) signaling by calpain-generated free catalytic domains induces HDAC5 nuclear export and regulates cardiac transcription
    Yan Zhang
    Center for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 286:26943-51. 2011
    ....
  24. ncbi Clinical and genetic modifiers of long-term survival in heart failure
    Sharon Cresci
    Center for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Am Coll Cardiol 54:432-44. 2009
    ..This study sought to identify genetic modifiers of beta-blocker response and long-term survival in heart failure (HF)...
  25. ncbi The human G147D-protein phosphatase 1 inhibitor-1 polymorphism is not associated with altered clinical characteristics in heart failure
    Guoli Chen
    Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267 0575, USA
    Cardiology 112:224-31. 2009
    ..The present study sought to examine whether the G147D inhibitor-1 polymorphism may be associated with specific clinical characteristics of heart failure carriers...
  26. ncbi A GRK5 polymorphism that inhibits beta-adrenergic receptor signaling is protective in heart failure
    Stephen B Liggett
    Department of Internal Medicine, University of Cincinnati, 231 Albert Sabin Way, Cincinnati, Ohio 45267, USA
    Nat Med 14:510-7. 2008
    ....
  27. ncbi The presence of Lys27 instead of Asn27 in human phospholamban promotes sarcoplasmic reticulum Ca2+-ATPase superinhibition and cardiac remodeling
    Wen Zhao
    Department of Pharmacology, University of Cincinnati College of Medicine, Cincinnati, OH 45267 0575, USA
    Circulation 113:995-1004. 2006
    ..The amino acid sequence of PLN is highly conserved, and although all species contain asparagine (Asn), human PLN is unique in containing lysine (Lys) at amino acid 27...
  28. ncbi Regulation of cardiac contractility by Rab4-modulated beta2-adrenergic receptor recycling
    Amy Odley
    Heart and Vascular Center, University of Cincinnati, Cincinnati, OH 45267, USA
    Proc Natl Acad Sci U S A 101:7082-7. 2004
    ....
  29. ncbi MARF and Opa1 control mitochondrial and cardiac function in Drosophila
    Gerald W Dorn
    Center for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA
    Circ Res 108:12-7. 2011
    ..The role of mitochondrial fusion in functioning of the heart, where mitochondria comprise ≈30% of cardiomyocyte volume and their intermyofilament spatial arrangement with other mitochondria is highly ordered, is unknown...
  30. ncbi A functional polymorphism of the Galphaq (GNAQ) gene is associated with accelerated mortality in African-American heart failure
    Stephen B Liggett
    Department of Medicine, Cardiopulmonary Genomics Program, University of Maryland, Baltimore, MD, USA
    Hum Mol Genet 16:2740-50. 2007
    ..Thus, the GNAQ -694/-695 promoter polymorphism alters transcription factor binding, increases promoter activity and adversely affects outcome in human heart failure...
  31. ncbi Proapoptotic effects of caspase-1/interleukin-converting enzyme dominate in myocardial ischemia
    Faisal M Syed
    Department of Medicine, University of Cincinnati, Cincinnati, Ohio, USA
    Circ Res 96:1103-9. 2005
    ....
  32. ncbi Mediating ERK 1/2 signaling rescues congenital heart defects in a mouse model of Noonan syndrome
    Tomoki Nakamura
    Cincinnati Children s Hospital Medical Center, The Children s Hospital Research Foundation, Division of Molecular Cardiovascular Biology, Cincinnati, Ohio 45229 3039, USA
    J Clin Invest 117:2123-32. 2007
    ....
  33. ncbi Nuclear effects of G-protein receptor kinase 5 on histone deacetylase 5-regulated gene transcription in heart failure
    Yan Zhang
    Center for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, St Louis, MO, USA
    Circ Heart Fail 4:659-68. 2011
    ..GRK5 is distinguished by partial nuclear localization and class II histone deacetylases (HDAC) kinase activity that is postulated to regulate Gαq-stimulated cardiac gene expression...
  34. ncbi Unrestrained erythroblast development in Nix-/- mice reveals a mechanism for apoptotic modulation of erythropoiesis
    Abhinav Diwan
    Center for Molecular Cardiovascular Research and Department of Pediatrics, Children s Hospital Medical Center, University of Cincinnati, Cincinnati, OH 45267, USA
    Proc Natl Acad Sci U S A 104:6794-9. 2007
    ..These results suggest that physiological codependence and coordinated regulation of pro- and antiapoptotic Bcl2 family members may represent a general regulatory paradigm in hematopoiesis...
  35. ncbi Cardiac-specific ablation of G-protein receptor kinase 2 redefines its roles in heart development and beta-adrenergic signaling
    Scot J Matkovich
    Center for Molecular Cardiovascular Research, University of Cincinnati, Ohio, USA
    Circ Res 99:996-1003. 2006
    ..In the adult heart, cardiac GRK2 is a major factor regulating inotropic and lusitropic tachyphylaxis to beta-adrenergic agonist, which likely contributes to its protective effects in catecholamine cardiomyopathy...
  36. ncbi Distinct pathways regulate proapoptotic Nix and BNip3 in cardiac stress
    Anita S Galvez
    Department of Internal Medicine, University of Cincinnati, Cincinnati Ohio 45267 0542, USA
    J Biol Chem 281:1442-8. 2006
    ..BNip3 is hypoxia-inducible, whereas Nix expression was induced by G alpha(q)-mediated hypertrophic stimuli. PKC alpha, a G(q) effector, transduced Nix transcriptional induction via Sp1...
  37. ncbi Adrenergic-pathway gene variants influence beta-blocker-related outcomes after acute coronary syndrome in a race-specific manner
    Sharon Cresci
    Department of Medicine, Washington University School of Medicine, St Louis, Missouri, USA
    J Am Coll Cardiol 60:898-907. 2012
    ..Whether these genetic variants are associated with survival among ACS patients treated with BB, and if this differs by race, is unknown...
  38. ncbi Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death
    Christopher P Baines
    Department of Pediatrics, Children s Hospital Medical Center, Cincinnati, Ohio 45229, USA
    Nature 434:658-62. 2005
    ..Thus, cyclophilin D and the mitochondrial permeability transition are required for mediating Ca2+- and oxidative damage-induced cell death, but not Bcl-2 family member-regulated death...
  39. ncbi Loss of Nix in Pdx1-deficient mice prevents apoptotic and necrotic β cell death and diabetes
    Kei Fujimoto
    Division of Endocrinology, Metabolism and Lipid Research, Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Clin Invest 120:4031-9. 2010
    ..These results establish Nix as a critical mediator of β cell apoptosis and programmed necrosis in Pdx1-deficient diabetes...
  40. ncbi Manipulating cardiac contractility in heart failure: data from mice and men
    Gerald W Dorn
    Department of Internal Medicine, Division of Cardiology, University of Cincinnati Medical Center, Cincinnati, Ohio, USA
    Circulation 109:150-8. 2004
  41. ncbi Association of an intronic, but not any exonic, FRMD4B sequence variant and heart failure
    Scot J Matkovich
    The Center for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, St Louis, Missouri, USA
    Clin Transl Sci 3:134-9. 2010
    ....
  42. ncbi Deep mRNA sequencing for in vivo functional analysis of cardiac transcriptional regulators: application to Galphaq
    Scot J Matkovich
    Department of Medicine, Center for Pharmacogenomics, Washington University School of Medicine, St Louis, MO 63110, USA
    Circ Res 106:1459-67. 2010
    ..Transcriptional profiling can detect subclinical heart disease and provide insight into disease etiology and functional status. Current microarray-based methods are expensive and subject to artifact...
  43. ncbi Cardiac signaling genes exhibit unexpected sequence diversity in sporadic cardiomyopathy, revealing HSPB7 polymorphisms associated with disease
    Scot J Matkovich
    Center for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, 660 S Eucliud Avenue, St Louis, Missouri 63110, USA
    J Clin Invest 120:280-9. 2010
    ....
  44. ncbi RISC RNA sequencing for context-specific identification of in vivo microRNA targets
    Scot J Matkovich
    Center for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA
    Circ Res 108:18-26. 2011
    ..One miR can target hundreds of individual mRNAs, but existing methodologies are not sufficient to accurately and comprehensively identify these mRNA targets in vivo...
  45. ncbi An FHL1-containing complex within the cardiomyocyte sarcomere mediates hypertrophic biomechanical stress responses in mice
    Farah Sheikh
    Department of Medicine, UCSD, La Jolla, California 92093, USA
    J Clin Invest 118:3870-80. 2008
    ..These studies shed light on the physiological regulation of the sarcomere in response to hypertrophic stress...
  46. ncbi 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
    ....
  47. ncbi Human phospholamban null results in lethal dilated cardiomyopathy revealing a critical difference between mouse and human
    Kobra Haghighi
    Department of Pharmacology and Cell Biophysics, University of Cincinnati, College of Medicine, Cincinnati, Ohio 45267, USA
    J Clin Invest 111:869-76. 2003
    ..These findings describe a naturally-occurring loss-of-function human PLN mutation (PLN null). In contrast to reported benefits of PLN ablation in mouse heart failure, humans lacking PLN develop lethal dilated cardiomyopathy...
  48. ncbi Pharmacogenetic profiling in the treatment of heart disease
    Gerald W Dorn
    Center for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, St Louis, MO, USA
    Transl Res 154:295-302. 2009
    ....
  49. ncbi Beta 1-adrenergic receptor polymorphisms confer differential function and predisposition to heart failure
    Jeanne Mialet Perez
    Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA
    Nat Med 9:1300-5. 2003
    ....
  50. ncbi Inhibition of cardiac myocyte apoptosis improves cardiac function and abolishes mortality in the peripartum cardiomyopathy of Galpha(q) transgenic mice
    Yukihiro Hayakawa
    Program in Molecular Cardiology, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Circulation 108:3036-41. 2003
    ..These data indicate that cardiac myocyte apoptosis plays a causal role in the pathogenesis of cardiomyopathy in this model. Caspase inhibition may provide a novel therapeutic target for heart failure...
  51. ncbi Polymorphic SERCA2a variants do not account for inter-individual differences in phospholamban-SERCA2a interactions in human heart failure
    Albrecht G Schmidt
    Department of Pharmacology and Cell Biophysics, University of Cincinnati Medical Center, 231 Albert Sabin Way, ML 0575, Cincinnati, OH 45267, USA
    J Mol Cell Cardiol 35:867-70. 2003
  52. ncbi Abnormal neurodevelopment, neurosignaling and behaviour in Npas3-deficient mice
    Eric W Brunskill
    Division of Cardiology, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267, USA
    Eur J Neurosci 22:1265-76. 2005
    ..Together, our observations indicate an important role for Npas3 in controlling normal brain development and neurosignaling pathways...
  53. ncbi Periostin and myocardial repair, regeneration, and recovery
    Gerald W Dorn
    Center for Molecular Cardiovascular Research, University of Cincinnati, Cincinnati, USA
    N Engl J Med 357:1552-4. 2007
  54. ncbi Bax regulates primary necrosis through mitochondrial dynamics
    Russell S Whelan
    Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 109:6566-71. 2012
    ..Thus, Bax and Bak play wider roles in cell death than previously appreciated and may be optimal therapeutic targets for diseases that involve both forms of cell death...
  55. ncbi Rescue of cardiomyocyte dysfunction by phospholamban ablation does not prevent ventricular failure in genetic hypertrophy
    Qiujing Song
    Department of Pharmacology and Cell Biophysics, University of Cincinnati Medical Center, Cincinnati, Ohio 45267, USA
    J Clin Invest 111:859-67. 2003
    ..Thus, PLN ablation normalized contractility in isolated myocytes, but failed to rescue the cardiomyopathic phenotype elicited by activation of the Galphaq pathway or MyBP-C mutations...
  56. ncbi MicroRNAs in cardiac disease
    Gerald W Dorn
    Center for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, Saint Louis, MO, USA
    Transl Res 157:226-35. 2011
    ..These advances establish a foundation for novel diagnostics and new therapeutic approaches for myocardial infarction, cardiac hypertrophy, and heart failure...
  57. ncbi Decompensation of cardiac hypertrophy: cellular mechanisms and novel therapeutic targets
    Abhinav Diwan
    Center for Molecular Cardiovascular Research, University of Cincinnati, Cincinnati, OH, USA
    Physiology (Bethesda) 22:56-64. 2007
    ..The rational application of these mechanistic considerations to therapeutics targeting hypertrophy and heart failure is discussed...
  58. ncbi Ischemic protection and myofibrillar cardiomyopathy: dose-dependent effects of in vivo deltaPKC inhibition
    Harvey S Hahn
    Department of Internal Medicine, Division of Cardiology, University of Cincinnati Medical Center, Cincinnati, Ohio 45267 0542, USA
    Circ Res 91:741-8. 2002
    ....
  59. ncbi Physiologic growth and pathologic genes in cardiac development and cardiomyopathy
    Gerald W Dorn
    Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati, 231 Albert Sabin Lane, Cincinnati, OH 45267 0542, USA
    Trends Cardiovasc Med 15:185-9. 2005
    ..Here, studies of Galphaq and Nix, powerful signaling factors for pathologic hypertrophy and cardiomyocyte apoptosis, respectively, are reviewed in terms of their comparative effects on cardiac development and adult cardiac pathology...
  60. ncbi Mitochondrial death protein Nix is induced in cardiac hypertrophy and triggers apoptotic cardiomyopathy
    Martin G Yussman
    Department of Internal Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio, USA
    Nat Med 8:725-30. 2002
    ..Thus, Nix/Bnip3L is upregulated in myocardial hypertrophy, and is both necessary and sufficient for Gq-mediated apoptosis of cardiomyocytes and resulting hypertrophy decompensation...
  61. ncbi MicroRNAs: redefining mechanisms in cardiac disease
    Gerald W Dorn
    Center for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, St Louis, MO, USA
    J Cardiovasc Pharmacol 56:589-95. 2010
    ....
  62. ncbi Adrenergic pathways and left ventricular remodeling
    Gerald W Dorn
    Department of Medicine, University of Cincinnati, Cincinnati, Ohio 45267-0542, USA
    J Card Fail 8:S370-3. 2002
    ..These effects of beta-adrenergic receptors are concentration-dependent, and appear to be much more severe for the beta 1 than the beta 2 subtype, perhaps because of beta 2 coupling to inhibitory Gi...
  63. ncbi Signaling pathways involved in left ventricular remodeling: summation
    Gerald W Dorn
    Section of Cardiology, Department of Medicine, University of Cincinnati, Cincinnati, Ohio, USA
    J Card Fail 8:S387-8. 2002
  64. ncbi Transforming growth factor beta in cardiovascular development and function
    Mohamad Azhar
    Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    Cytokine Growth Factor Rev 14:391-407. 2003
    ..The evidence for TGFbeta activities during cardiovascular development and physiologic function will be given and areas which need further investigation will be discussed...
  65. ncbi RAS point mutations and PAX8-PPAR gamma rearrangement in thyroid tumors: evidence for distinct molecular pathways in thyroid follicular carcinoma
    Marina N Nikiforova
    Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio 45267 0529, USA
    J Clin Endocrinol Metab 88:2318-26. 2003
    ..These results suggest that conventional follicular thyroid carcinomas develop through at least two distinct and virtually nonoverlapping molecular pathways initiated by either RAS point mutation or PAX8-PPAR gamma rearrangement...
  66. ncbi Protein kinase D links Gq-coupled receptors to cAMP response element-binding protein (CREB)-Ser133 phosphorylation in the heart
    Nazira Ozgen
    Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    J Biol Chem 283:17009-19. 2008
    ....
  67. ncbi Histidine-rich Ca binding protein: a regulator of sarcoplasmic reticulum calcium sequestration and cardiac function
    Kimberly N Gregory
    Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, OH 45267 0575, USA
    J Mol Cell Cardiol 40:653-65. 2006
    ..Collectively, these data suggest that HRC may be an integral regulatory protein involved in cardiac muscle SR Ca uptake and Ca homeostasis...
  68. ncbi Cardiac myosin-binding protein-C phosphorylation and cardiac function
    Sakthivel Sadayappan
    Division of Molecular Cardiovascular Biology, Department of Pediatrics, Cincinnati Children s Hospital Medical Center, OH, USA
    Circ Res 97:1156-63. 2005
    ..In contrast, when the MyBP-C(t/t) mice were bred to a TG line expressing normal MyBP-C (MyBP-CWT), the MyBP-C(t/t) phenotype was rescued. These data suggest that cMyBP-C phosphorylation is essential for normal cardiac function...
  69. ncbi Inhibition of apoptosis-regulated signaling kinase-1 and prevention of congestive heart failure by estrogen
    Minoru Satoh
    Vascular Medicine Research Unit, Brigham and Women s Hospital and Harvard Medical School, Cambridge, MA 02139, USA
    Circulation 115:3197-204. 2007
    ..We hypothesize that estrogen prevents cardiomyocyte apoptosis and the development of CHF...
  70. ncbi Ca2+ dysregulation induces mitochondrial depolarization and apoptosis: role of Na+/Ca2+ exchanger and AKT
    Shigeki Miyamoto
    Department of Pharmacology, University of California San Diego, La Jolla, California 92093, USA
    J Biol Chem 280:38505-12. 2005
    ....
  71. ncbi Additive protection of the ischemic heart ex vivo by combined treatment with delta-protein kinase C inhibitor and epsilon-protein kinase C activator
    Koichi Inagaki
    Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, Calif 94305-5174, USA
    Circulation 108:869-75. 2003
    ..Furthermore, treatment with both peptides confers additive cardioprotective effects. Therefore, these peptides mediate cardioprotection by regulating ischemia/reperfusion damage at distinct time points...
  72. ncbi Disruption of ROCK1 gene attenuates cardiac dilation and improves contractile function in pathological cardiac hypertrophy
    Jianjian Shi
    Herman B Wells Center for Pediatric Research, Division of Pediatric Cardiology, Department of Pediatrics, Indiana University, School of Medicine, Indianapolis, IN, USA
    J Mol Cell Cardiol 44:551-60. 2008
    ..The present study establishes for the first time a role for ROCK1 in cardiac dilation and contractile dysfunction...
  73. ncbi Physiological growth synergizes with pathological genes in experimental cardiomyopathy
    Faisal Syed
    Heart and Vascular Center of the University of Cincinnati, Ohio 45267-0542, USA
    Circ Res 95:1200-6. 2004
    ..Thus, normal postnatal cardiac growth can be an essential cofactor in development of genetic cardiomyopathies, and may confound the interpretation of conventional alpha-MHC transgenic phenotypes...
  74. ncbi Phenotyping hypertrophy: eschew obfuscation
    Gerald W Dorn
    Circ Res 92:1171-5. 2003
  75. ncbi Containing hypertrophy with a PICOT fence
    Gerald W Dorn
    Circ Res 99:228-30. 2006
  76. ncbi MicroRNA-133 controls cardiac hypertrophy
    Alessandra Carè
    Department of Hematology, Oncology and Molecular Medicine, Istituto Superiore Sanita, 00161 Rome, Italy
    Nat Med 13:613-8. 2007
    ..Our data show that miR-133, and possibly miR-1, are key regulators of cardiac hypertrophy, suggesting their therapeutic application in heart disease...

Research Grants3

  1. G-Protein Receptor Kinases in Cardiac Stress Adaptation
    GERALD DORN; Fiscal Year: 2007
    ....
  2. Calpains as Mediators of Cardiac Ischemic Injury
    GERALD DORN; Fiscal Year: 2007
    ..Collectively, these studies will apply state-of-the-art techniques for in vivo genetic manipulation, microphysiologic analysis, and biochemical assessment to achieve insight into the roles of myocardial calpains in health and disease. ..
  3. Core--Clinical Research Skills Development
    GERALD DORN; Fiscal Year: 2007
    ..abstract_text> ..