James Tidball

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi request reprint Calpains and muscular dystrophies
    J G Tidball
    Department of Physiological Science, Duchenne Muscular Dystrophy Research Center, University of California, Los Angeles 90095, USA
    Int J Biochem Cell Biol 32:1-5. 2000
  2. doi request reprint Mechanisms of muscle injury, repair, and regeneration
    James G Tidball
    Molecular, Cellular and Integrative Physiology Program, University of California, Los Angeles, California, USA
    Compr Physiol 1:2029-62. 2011
  3. pmc Regulatory interactions between muscle and the immune system during muscle regeneration
    James G Tidball
    Molecular, Cellular and Integrative Physiology Program, Department of Integrative Biology and Physiology, University of California Los Angeles, CA 90095 1606, USA
    Am J Physiol Regul Integr Comp Physiol 298:R1173-87. 2010
  4. ncbi request reprint The role of free radicals in the pathophysiology of muscular dystrophy
    James G Tidball
    Department of Physiological Science, University of California, Los Angeles, California 90095, USA
    J Appl Physiol 102:1677-86. 2007
  5. pmc Macrophages promote muscle membrane repair and muscle fibre growth and regeneration during modified muscle loading in mice in vivo
    James G Tidball
    Department of Physiological Science, 5833 Life Science Building, University of California, Los Angeles, CA 90095, USA
    J Physiol 578:327-36. 2007
  6. ncbi request reprint Damage and inflammation in muscular dystrophy: potential implications and relationships with autoimmune myositis
    James G Tidball
    Department of Physiological Science, University of California, Los Angeles, California 90095, USA
    Curr Opin Rheumatol 17:707-13. 2005
  7. ncbi request reprint Mechanical signal transduction in skeletal muscle growth and adaptation
    James G Tidball
    Department of Physiological Science, 5833 Life Science Bldg, University of California, Los Angeles, CA 90095, USA
    J Appl Physiol 98:1900-8. 2005
  8. ncbi request reprint Inflammatory processes in muscle injury and repair
    James G Tidball
    Department of Physiological Science, 5833 Life Science Bldg, University of California, Los Angeles, CA 90095, USA
    Am J Physiol Regul Integr Comp Physiol 288:R345-53. 2005
  9. ncbi request reprint Evolving therapeutic strategies for Duchenne muscular dystrophy: targeting downstream events
    James G Tidball
    Department of Physiological Science, University of California, Los Angeles, CA 90095, USA
    Pediatr Res 56:831-41. 2004
  10. ncbi request reprint Expression of a NOS transgene in dystrophin-deficient muscle reduces muscle membrane damage without increasing the expression of membrane-associated cytoskeletal proteins
    James G Tidball
    Department of Physiological Science, University of California, Los Angeles, CA 90095, USA
    Mol Genet Metab 82:312-20. 2004

Research Grants

Collaborators

  • Tomomi Gotoh
  • Aldons Jake Lusis
  • MELISSA JAN SPENCER
  • Wayne W Grody
  • Hal X Nguyen
  • PAULUS JANSSEN
  • Jurgen Radons
  • Michael Karin
  • Z Sahenk
  • ALADIN BORIEK
  • Denis C Guttridge
  • Michelle Wehling-Henricks
  • Bo Deng
  • S Armando Villalta
  • Kyu H Myung
  • Minqi Hao
  • Kenneth P Roos
  • Maria C Jordan
  • Karin Pfister
  • Swarnali Acharyya
  • Terry Shiao
  • Brian A Kyckelhahn
  • David Glanzman
  • Chiara Rinaldi
  • Meredith Oltmann
  • Ke Wei
  • Carlos de Diego
  • Jamie J Lee
  • Fabian Chen
  • Michael C Graves
  • Perry B Shieh
  • Jeong Hee Ku
  • Kevan Akrami
  • Nam Che
  • Sophie Sokolow
  • Horst J├╝rgen Feldmann
  • Raymonde Busch
  • Jill A Rafael-Fortney
  • Gabriele Multhoff
  • Katherine L Gardner
  • Micheal Carathers
  • Sankar Ghosh
  • Michael Pfeifer
  • Nadine Bakkar
  • Amer A Beg
  • Albert S Baldwin
  • Tepmanas Bupha-Intr
  • Zhi Wei Li
  • Michael Weinstein
  • Valeria Milani
  • Rolf Issels
  • Lutz Freitag
  • Stanley C Froehner
  • Marvin E Adams
  • James J Lee
  • Andrew Fond
  • Patricia B Nason

Detail Information

Publications30

  1. ncbi request reprint Calpains and muscular dystrophies
    J G Tidball
    Department of Physiological Science, Duchenne Muscular Dystrophy Research Center, University of California, Los Angeles 90095, USA
    Int J Biochem Cell Biol 32:1-5. 2000
    ..Thus, modulation of calpain activity or expression through pharmacological or molecular genetic approaches may provide therapies for some muscular dystrophies...
  2. doi request reprint Mechanisms of muscle injury, repair, and regeneration
    James G Tidball
    Molecular, Cellular and Integrative Physiology Program, University of California, Los Angeles, California, USA
    Compr Physiol 1:2029-62. 2011
    ....
  3. pmc Regulatory interactions between muscle and the immune system during muscle regeneration
    James G Tidball
    Molecular, Cellular and Integrative Physiology Program, Department of Integrative Biology and Physiology, University of California Los Angeles, CA 90095 1606, USA
    Am J Physiol Regul Integr Comp Physiol 298:R1173-87. 2010
    ..Together, these findings show that transitions in macrophage phenotype are an essential component of muscle regeneration in vivo following acute or chronic muscle damage...
  4. ncbi request reprint The role of free radicals in the pathophysiology of muscular dystrophy
    James G Tidball
    Department of Physiological Science, University of California, Los Angeles, California 90095, USA
    J Appl Physiol 102:1677-86. 2007
    ..More mechanistic knowledge of the specific disruptions of free radicals that underlie major features of muscular dystrophy is needed to develop more targeted and successful therapeutic approaches...
  5. pmc Macrophages promote muscle membrane repair and muscle fibre growth and regeneration during modified muscle loading in mice in vivo
    James G Tidball
    Department of Physiological Science, 5833 Life Science Building, University of California, Los Angeles, CA 90095, USA
    J Physiol 578:327-36. 2007
    ..These findings collectively show that macrophages play a significant role in muscle fibre membrane repair, regeneration and growth during increased muscle use after a period of atrophy...
  6. ncbi request reprint Damage and inflammation in muscular dystrophy: potential implications and relationships with autoimmune myositis
    James G Tidball
    Department of Physiological Science, University of California, Los Angeles, California 90095, USA
    Curr Opin Rheumatol 17:707-13. 2005
    ..Recent findings are summarized which indicate that immune-targeted interventions may provide useful approaches to treat muscular dystrophy...
  7. ncbi request reprint Mechanical signal transduction in skeletal muscle growth and adaptation
    James G Tidball
    Department of Physiological Science, 5833 Life Science Bldg, University of California, Los Angeles, CA 90095, USA
    J Appl Physiol 98:1900-8. 2005
    ....
  8. ncbi request reprint Inflammatory processes in muscle injury and repair
    James G Tidball
    Department of Physiological Science, 5833 Life Science Bldg, University of California, Los Angeles, CA 90095, USA
    Am J Physiol Regul Integr Comp Physiol 288:R345-53. 2005
    ....
  9. ncbi request reprint Evolving therapeutic strategies for Duchenne muscular dystrophy: targeting downstream events
    James G Tidball
    Department of Physiological Science, University of California, Los Angeles, CA 90095, USA
    Pediatr Res 56:831-41. 2004
    ..Each of these general approaches to slowing the pathology of dystrophin deficiency has yielded encouragement and suggests that targeting downstream events in dystrophinopathy can yield worthwhile, functional improvements in DMD...
  10. ncbi request reprint Expression of a NOS transgene in dystrophin-deficient muscle reduces muscle membrane damage without increasing the expression of membrane-associated cytoskeletal proteins
    James G Tidball
    Department of Physiological Science, University of California, Los Angeles, CA 90095, USA
    Mol Genet Metab 82:312-20. 2004
    ..Together, these findings indicate that the NOS transgene does not reduce dystrophinopathy by increasing the expression of compensatory, structural proteins...
  11. ncbi request reprint Macrophage invasion does not contribute to muscle membrane injury during inflammation
    J G Tidball
    Department of Physiological Science, University of California, Los Angeles 90095 1527, USA
    J Leukoc Biol 65:492-8. 1999
    ..Thus, muscle invasion by neutrophils is not sufficient to cause invasion by ED1+ macrophages. In addition, muscle membrane injury that occurs during reloading is independent of invasion by ED1+ macrophages...
  12. ncbi request reprint Nitric-oxide synthase is a mechanical signal transducer that modulates talin and vinculin expression
    J G Tidball
    Department of Physiological Science, University of California, Los Angeles, California 90095 1527, USA
    J Biol Chem 274:33155-60. 1999
    ....
  13. pmc Expression of a calpastatin transgene slows muscle wasting and obviates changes in myosin isoform expression during murine muscle disuse
    James G Tidball
    Department of Physiological Science, David Geffen School of Medicine at UCLA, 5833 Life Science Building, Los Angeles, CA 90095, USA
    J Physiol 545:819-28. 2002
    ..These findings indicate that therapeutics directed toward regulating the calpain-calpastatin system may be beneficial in preventing muscle mass loss in muscle injury and disease...
  14. pmc Expression of a muscle-specific, nitric oxide synthase transgene prevents muscle membrane injury and reduces muscle inflammation during modified muscle use in mice
    Hal X Nguyen
    Department of Physiological Science, University of California, Los Angeles, CA 90095, USA
    J Physiol 550:347-56. 2003
    ..Together, these data show that muscle-derived NO can function as an anti-inflammatory molecule in muscle that experiences modified loading, and that NO can prevent neutrophil-mediated damage of muscle cell membranes in vivo and in vitro...
  15. ncbi request reprint Defects in neuromuscular junction structure in dystrophic muscle are corrected by expression of a NOS transgene in dystrophin-deficient muscles, but not in muscles lacking alpha- and beta1-syntrophins
    Terry Shiao
    Department of Physiological Science, University of California, Los Angeles 90095, USA
    Hum Mol Genet 13:1873-84. 2004
    ..The results suggest that defects in NMJ structure that occur in some DGC mutants can result from the secondary loss of NOS from muscle...
  16. pmc Shifts in macrophage phenotypes and macrophage competition for arginine metabolism affect the severity of muscle pathology in muscular dystrophy
    S Armando Villalta
    Molecular, Cellular and Integrative Physiology Program, David Geffen School of Medicine at UCLA, University of California, Los Angeles, CA 90095 1606, USA
    Hum Mol Genet 18:482-96. 2009
    ....
  17. pmc Nitric oxide generated by muscle corrects defects in hippocampal neurogenesis and neural differentiation caused by muscular dystrophy
    Bo Deng
    Molecular, Cellular and Integrative Physiology Program, University of California, Los Angeles, CA 90095 1606, USA
    J Physiol 587:1769-78. 2009
    ..These findings indicate that muscle-derived NO regulates adult neurogenesis in the brain and loss of muscle nNOS may underlie defects in the central nervous system in DMD...
  18. pmc Major basic protein-1 promotes fibrosis of dystrophic muscle and attenuates the cellular immune response in muscular dystrophy
    Michelle Wehling-Henricks
    Department of Physiological Science, David Geffen School of Medicine at UCLA, University of California, Los Angeles, CA90095 1606, USA
    Hum Mol Genet 17:2280-92. 2008
    ....
  19. ncbi request reprint Prednisolone decreases cellular adhesion molecules required for inflammatory cell infiltration in dystrophin-deficient skeletal muscle
    Michelle Wehling-Henricks
    Department of Physiological Science, University of California, 5833 Life Science Building, Los Angeles, CA 90095 1527, USA
    Neuromuscul Disord 14:483-90. 2004
    ..Prednisolone reduced sarcolemmal damage and degeneration as well. Our data show that prednisolone is an effective anti-inflammatory in dystrophic muscle and may function by modulating CAM expression...
  20. pmc Null mutation of myeloperoxidase in mice prevents mechanical activation of neutrophil lysis of muscle cell membranes in vitro and in vivo
    Hal X Nguyen
    Department of Physiological Science, 5833 Life Science Building, University of California, Los Angeles, CA 90095, USA
    J Physiol 565:403-13. 2005
    ..Together, these in vitro and in vivo findings show that mechanical loading activates neutrophil-mediated lysis of muscle cells through an MPO-dependent pathway...
  21. pmc Loss of positive allosteric interactions between neuronal nitric oxide synthase and phosphofructokinase contributes to defects in glycolysis and increased fatigability in muscular dystrophy
    Michelle Wehling-Henricks
    Department of Physiological Science, David Geffen School of Medicine, University of California, Los Angeles, CA 90095 1606, USA
    Hum Mol Genet 18:3439-51. 2009
    ..Collectively, these findings indicate that defects in glycolytic metabolism and increased fatigability in dystrophic muscle may be caused in part by the loss of positive allosteric interactions between nNOS and PFK...
  22. pmc Arginine metabolism by macrophages promotes cardiac and muscle fibrosis in mdx muscular dystrophy
    Michelle Wehling-Henricks
    Department of Integrative Biology and Physiology, University of California Los Angeles, Los Angeles, California, USA
    PLoS ONE 5:e10763. 2010
    ....
  23. ncbi request reprint Cardiomyopathy in dystrophin-deficient hearts is prevented by expression of a neuronal nitric oxide synthase transgene in the myocardium
    Michelle Wehling-Henricks
    Department of Physiological Science, David Geffen School of Medicine, University of California, Los Angeles 90095, USA
    Hum Mol Genet 14:1921-33. 2005
    ..These findings indicate that increasing NO production by dystrophic hearts may have therapeutic value...
  24. doi request reprint Muscleblind-like 2 (Mbnl2) -deficient mice as a model for myotonic dystrophy
    Minqi Hao
    Department of Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095 1760, USA
    Dev Dyn 237:403-10. 2008
    ..Our results support the hypothesis that Muscleblind proteins and specifically MBNL2 contribute to the pathogenesis of human DM...
  25. pmc Interplay of IKK/NF-kappaB signaling in macrophages and myofibers promotes muscle degeneration in Duchenne muscular dystrophy
    Swarnali Acharyya
    Human Cancer Genetics Program and Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University College of Medicine, Columbus, Ohio 43210, USA
    J Clin Invest 117:889-901. 2007
    ..Collectively, these results underscore the critical role of NF-kappaB in the progression of muscular dystrophy and suggest the IKK/NF-kappaB signaling pathway as a potential therapeutic target for DMD...
  26. pmc Null mutation of gp91phox reduces muscle membrane lysis during muscle inflammation in mice
    Hal X Nguyen
    Departments of Physiological Science
    J Physiol 553:833-41. 2003
    ....
  27. pmc Interactions between neutrophils and macrophages promote macrophage killing of rat muscle cells in vitro
    Hal X Nguyen
    Department of Physiological Science, University of California, Los Angeles, CA 90095, USA
    J Physiol 547:125-32. 2003
    ....
  28. ncbi request reprint Kinematic modeling of single muscle fiber during diaphragm shortening
    Brian A Kyckelhahn
    Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA
    J Biomech 36:457-61. 2003
    ..The model that matches physiologic data best has zero transverse strain and has a relationship between fiber shape and muscle shortening consistent with published data on single muscle fiber mechanics...
  29. ncbi request reprint Skipping to new gene therapies for muscular dystrophy
    James G Tidball
    Nat Med 9:997-8. 2003
  30. ncbi request reprint Patient survival by Hsp70 membrane phenotype: association with different routes of metastasis
    Karin Pfister
    Department for Surgery, University Hospital Regensburg, Regensburg, Germany
    Cancer 110:926-35. 2007
    ..The authors prospectively investigated the correlation between the tumor-specific Hsp70 membrane expression as an independent clinicopathological marker and overall survival in tumor entities that differ in their route of metastasis...

Research Grants35

  1. Myeloid Cell Function in Muscle Injury and Repair
    James Tidball; Fiscal Year: 2005
    ..Those findings can indicate new therapeutic approaches to improving muscle function during muscle reloading following periods of reduced loading. ..
  2. Myeloid Cell Function in Muscular Dystrophy
    James Tidball; Fiscal Year: 2005
    ..Results of the study proposed here will permit us to determine whether therapeutic approaches that are based on reducing myeloid cell mediated pathology can be productive approaches to the treatment of these forms of muscular dystrophy. ..
  3. Training in Molecular, Cellular & Integrative Physiology
    James Tidball; Fiscal Year: 2007
    ..abstract_text> ..
  4. Myeloid Cell Function in Muscle Injury and Repair
    James G Tidball; Fiscal Year: 2010
    ..This study will yield the first mechanistic findings concerning macrophage function in muscle repair and growth during increased loading. ..
  5. Regulation of sarcopenia and muscle dysfunction by nitric oxide
    James G Tidball; Fiscal Year: 2010
    ..We anticipate that the results of this investigation can provide new insights into potential therapeutic strategies to reduce sarcopenia. ..
  6. Regulation of sarcopenia and muscle dysfunction by nitric oxide
    James Tidball; Fiscal Year: 2009
    ..We anticipate that the results of this investigation can provide new insights into potential therapeutic strategies to reduce sarcopenia. ..
  7. REGULATION OF MYOTENDINOUS JUNCTION STRUCTURE
    James Tidball; Fiscal Year: 1993
    ..The mechanism also will be examined in L6 rat myoblast using in vitro manipulations. The remodeling process will be examined using biochemical, immunological, morphological and biomechanical assays...
  8. MYOTENDINOUS JUNCTIONS--ADAPTATIONS TO EXERCISE
    James Tidball; Fiscal Year: 1991
    ....
  9. REGULATION OF MYOTENDINOUS JUNCTION STRUCTURE
    James Tidball; Fiscal Year: 2001
    ..Hind limb immobilization at shortened length followed by remobilization will be used to examine the effect of inhibition of NOS on sarcomere addition. ..
  10. Myeloid Cell Function in Muscle Injury and Repair
    James G Tidball; Fiscal Year: 2010
    ..This study will yield the first mechanistic findings concerning macrophage function in muscle repair and growth during increased loading. ..