CHRISTOPHER BAINES

Summary

Affiliation: University of Missouri
Country: USA

Publications

  1. ncbi Hypercholesterolemia increases mitochondrial oxidative stress and enhances the MPT response in the porcine myocardium: beneficial effects of chronic exercise
    Kyle S McCommis
    Dalton Cardiovascular Research Center, Univ of Missouri Columbia, 134 Research Park Dr, Columbia, MO 65211, USA
    Am J Physiol Regul Integr Comp Physiol 301:R1250-8. 2011
  2. ncbi How and when do myocytes die during ischemia and reperfusion: the late phase
    Christopher P Baines
    Department of Biomedical Sciences, and Dalton Cardiovascular Research Center, University of Missouri Columbia, Columbia, MO 65211, USA
    J Cardiovasc Pharmacol Ther 16:239-43. 2011
  3. ncbi The mitochondrial permeability transition pore and the cardiac necrotic program
    Christopher P Baines
    Department of Biomedical Sciences, Dalton Cardiovascular Research Center, University of Missouri Columbia, 134 Research Park Drive, Columbia, MO 65211, USA
    Pediatr Cardiol 32:258-62. 2011
  4. ncbi The cardiac mitochondrion: nexus of stress
    Christopher P Baines
    The Dalton Cardiovascular Research Center, Department of Biomedical Sciences, University of Missouri, Columbia, MO 65211, USA
    Annu Rev Physiol 72:61-80. 2010
  5. ncbi Adenine nucleotide translocase-1 induces cardiomyocyte death through upregulation of the pro-apoptotic protein Bax
    Christopher P Baines
    Department of Pediatrics, University of Cincinnati, Cincinnati Children s Hospital Medical Center, Cincinnati, OH 45229, USA
    J Mol Cell Cardiol 46:969-77. 2009
  6. ncbi Anti-hypertrophic effect of NHE-1 inhibition involves GSK-3beta-dependent attenuation of mitochondrial dysfunction
    Sabzali Javadov
    Department of Physiology and Pharmacology Schulich School of Medicine and Dentistry University of Western Ontario London, Ontario, Canada
    J Mol Cell Cardiol 46:998-1007. 2009
  7. ncbi The mitochondrial permeability transition pore and ischemia-reperfusion injury
    Christopher P Baines
    Department of Biomedical Sciences, Dalton Cardiovascular Research Center, University of Missouri Columbia, Columbia, MO 65211, USA
    Basic Res Cardiol 104:181-8. 2009
  8. ncbi The molecular composition of the mitochondrial permeability transition pore
    Christopher P Baines
    Department of Biomedical Sciences, Dalton Cardiovascular Research Center, University of Missouri Columbia, Columbia, Missouri 65211, USA
    J Mol Cell Cardiol 46:850-7. 2009
  9. ncbi The mitochondrial permeability transition pore as a target of cardioprotective signaling
    Christopher P Baines
    Department of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, MLC-7020, 3333 Burnet Ave, Cincinnati, OH 45229, USA
    Am J Physiol Heart Circ Physiol 293:H903-4. 2007
  10. ncbi Low-intensity aerobic interval training attenuates pathological left ventricular remodeling and mitochondrial dysfunction in aortic-banded miniature swine
    Craig A Emter
    Dept of Biomedical Science, Univ of Missouri, 1600 E Rollins, E117 Veterinary Medicine, Columbia, MO 65211, USA
    Am J Physiol Heart Circ Physiol 299:H1348-56. 2010

Research Grants

  1. Molecular Identity of the Cardiac Mitochondrial Pore
    CHRISTOPHER BAINES; Fiscal Year: 2009
  2. Molecular Identity of the Cardiac Mitochondrial Pore
    CHRISTOPHER PHILIP BAINES; Fiscal Year: 2010
  3. Molecular Identity of the Cardiac Mitochondrial Pore
    CHRISTOPHER PHILIP BAINES; Fiscal Year: 2011

Collaborators

  • Gerald W Dorn
  • Morris Karmazyn
  • Sabzali Javadov
  • Craig A Emter
  • Roberta A Gottlieb
  • Jeffery Molkentin
  • Elisabeth R Barton
  • Kyle S McCommis
  • Douglas P Millay
  • Jeffrey Robbins
  • Hiroyuki Nakayama
  • Abhinav Diwan
  • Douglas K Bowles
  • Allison M McGee
  • M Harold Laughlin
  • Michelle A Sargent
  • Gregoire Vuagniaux
  • Hanna Osinska
  • H Lee Sweeney
  • Hartmut Geiger
  • Andrew G Koesters
  • Suvarnamala Pushkaran
  • Theodosia A Kalfa
  • Kay F Macleod
  • Timothy E Hewett
  • Anil G Jegga
  • Xiongwen Chen
  • Balvin H L Chua
  • Raisa Klevitsky
  • Xiaoying Zhang
  • Diedre Daria
  • Steven R Houser
  • Amy M Odley
  • Hongyu Zhang
  • Benjamin T Spike
  • Bruce J Aronow
  • Naser Jaleel

Detail Information

Publications16

  1. ncbi Hypercholesterolemia increases mitochondrial oxidative stress and enhances the MPT response in the porcine myocardium: beneficial effects of chronic exercise
    Kyle S McCommis
    Dalton Cardiovascular Research Center, Univ of Missouri Columbia, 134 Research Park Dr, Columbia, MO 65211, USA
    Am J Physiol Regul Integr Comp Physiol 301:R1250-8. 2011
    ..We conclude that FH reduces mitochondrial antioxidants, increases mitochondrial oxidative stress, and enhances the MPT response in the porcine myocardium, and that exercise training can reverse these detrimental alterations...
  2. ncbi How and when do myocytes die during ischemia and reperfusion: the late phase
    Christopher P Baines
    Department of Biomedical Sciences, and Dalton Cardiovascular Research Center, University of Missouri Columbia, Columbia, MO 65211, USA
    J Cardiovasc Pharmacol Ther 16:239-43. 2011
    ....
  3. ncbi The mitochondrial permeability transition pore and the cardiac necrotic program
    Christopher P Baines
    Department of Biomedical Sciences, Dalton Cardiovascular Research Center, University of Missouri Columbia, 134 Research Park Drive, Columbia, MO 65211, USA
    Pediatr Cardiol 32:258-62. 2011
    ..Consequently, this report briefly reviews the roles of necrosis versus apoptosis in the pathogenesis of cardiac disease and discusses the role that the mitochondrial pore plays in cardiac necrotic cell death...
  4. ncbi The cardiac mitochondrion: nexus of stress
    Christopher P Baines
    The Dalton Cardiovascular Research Center, Department of Biomedical Sciences, University of Missouri, Columbia, MO 65211, USA
    Annu Rev Physiol 72:61-80. 2010
    ..The purpose of this review, therefore, is to focus on these mitochondrial mediators/inhibitors of cell death and to address the specific mechanisms that underlie their ability to influence cardiac pathology...
  5. ncbi Adenine nucleotide translocase-1 induces cardiomyocyte death through upregulation of the pro-apoptotic protein Bax
    Christopher P Baines
    Department of Pediatrics, University of Cincinnati, Cincinnati Children s Hospital Medical Center, Cincinnati, OH 45229, USA
    J Mol Cell Cardiol 46:969-77. 2009
    ..Taken together, these data indicate that ANT mediates cell death, not through the MPT pore, but rather via a ROS-dependent upregulation and activation of Bax...
  6. ncbi Anti-hypertrophic effect of NHE-1 inhibition involves GSK-3beta-dependent attenuation of mitochondrial dysfunction
    Sabzali Javadov
    Department of Physiology and Pharmacology Schulich School of Medicine and Dentistry University of Western Ontario London, Ontario, Canada
    J Mol Cell Cardiol 46:998-1007. 2009
    ..In conclusion, anti-hypertrophic effect of NHE-1 inhibition can be mediated through activation of GSK-3beta which in turn induces inhibition of mPTP opening due to VDAC phosphorylation...
  7. ncbi The mitochondrial permeability transition pore and ischemia-reperfusion injury
    Christopher P Baines
    Department of Biomedical Sciences, Dalton Cardiovascular Research Center, University of Missouri Columbia, Columbia, MO 65211, USA
    Basic Res Cardiol 104:181-8. 2009
    ..The purpose of this review is to focus on the role of the MPT pore in ischemia-reperfusion injury, the mechanisms involved, and, in particular, what we do and do not know regarding the pore's molecular composition...
  8. ncbi The molecular composition of the mitochondrial permeability transition pore
    Christopher P Baines
    Department of Biomedical Sciences, Dalton Cardiovascular Research Center, University of Missouri Columbia, Columbia, Missouri 65211, USA
    J Mol Cell Cardiol 46:850-7. 2009
    ..The purpose of this review is to outline our current understanding of the molecular identity of the MPT pore and the many questions that still need to be answered...
  9. ncbi The mitochondrial permeability transition pore as a target of cardioprotective signaling
    Christopher P Baines
    Department of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, MLC-7020, 3333 Burnet Ave, Cincinnati, OH 45229, USA
    Am J Physiol Heart Circ Physiol 293:H903-4. 2007
  10. ncbi Low-intensity aerobic interval training attenuates pathological left ventricular remodeling and mitochondrial dysfunction in aortic-banded miniature swine
    Craig A Emter
    Dept of Biomedical Science, Univ of Missouri, 1600 E Rollins, E117 Veterinary Medicine, Columbia, MO 65211, USA
    Am J Physiol Heart Circ Physiol 299:H1348-56. 2010
    ....
  11. ncbi Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death
    Christopher P Baines
    Department of Pediatrics, University of Cincinnati, Cincinnati Children s Hospital Medical Center, Cincinnati, OH 45229, USA
    Nat Cell Biol 9:550-5. 2007
    ..These results indicate that Vdacs are dispensable for both MPT and Bcl-2 family member-driven cell death...
  12. ncbi Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure
    Hiroyuki Nakayama
    Department of Pediatrics, Cincinnati Children s Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA
    J Clin Invest 117:2431-44. 2007
    ....
  13. 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...
  14. ncbi Genetic and pharmacologic inhibition of mitochondrial-dependent necrosis attenuates muscular dystrophy
    Douglas P Millay
    Department of Pediatrics, University of Cincinnati, Cincinnati Children s Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA
    Nat Med 14:442-7. 2008
    ..Thus, mitochondrial-dependent necrosis represents a prominent disease mechanism in muscular dystrophy, suggesting that inhibition of cyclophilin D could provide a new pharmacologic treatment strategy for these diseases...
  15. 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...
  16. ncbi STRESS signaling pathways that modulate cardiac myocyte apoptosis
    Christopher P Baines
    Division of Molecular Cardiovascular Biology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229-3039, USA
    J Mol Cell Cardiol 38:47-62. 2005
    ....

Research Grants3

  1. Molecular Identity of the Cardiac Mitochondrial Pore
    CHRISTOPHER BAINES; Fiscal Year: 2009
    ..Once the key proteins that mediate cell death are identified, they can then be targeted as a means of treating patients with heart disease. ..
  2. Molecular Identity of the Cardiac Mitochondrial Pore
    CHRISTOPHER PHILIP BAINES; Fiscal Year: 2010
    ..Once the key proteins that mediate cell death are identified, they can then be targeted as a means of treating patients with heart disease. ..
  3. Molecular Identity of the Cardiac Mitochondrial Pore
    CHRISTOPHER PHILIP BAINES; Fiscal Year: 2011
    ..Once the key proteins that mediate cell death are identified, they can then be targeted as a means of treating patients with heart disease. ..