Research Topics
| James TidballSummaryAffiliation: University of California Country: USA Publications
Research Grants
| Collaborators
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Detail Information
Publications
Calpains and muscular dystrophiesJ 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...- Macrophage invasion does not contribute to muscle membrane injury during inflammationJ 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... - Macrophages promote muscle membrane repair and muscle fibre growth and regeneration during modified muscle loading in mice in vivoJames 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... - Mechanical signal transduction in skeletal muscle growth and adaptationJames 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.... - The role of free radicals in the pathophysiology of muscular dystrophyJames 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... - Inflammatory processes in muscle injury and repairJames 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.... - Evolving therapeutic strategies for Duchenne muscular dystrophy: targeting downstream eventsJames 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... - Expression of a NOS transgene in dystrophin-deficient muscle reduces muscle membrane damage without increasing the expression of membrane-associated cytoskeletal proteinsJames 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... - Damage and inflammation in muscular dystrophy: potential implications and relationships with autoimmune myositisJames 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... - Regulatory interactions between muscle and the immune system during muscle regenerationJames 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... - Nitric-oxide synthase is a mechanical signal transducer that modulates talin and vinculin expressionJ G Tidball
Department of Physiological Science, University of California, Los Angeles, California 90095 1527, USA
J Biol Chem 274:33155-60. 1999.... - Expression of a calpastatin transgene slows muscle wasting and obviates changes in myosin isoform expression during murine muscle disuseJames 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... - 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-syntrophinsTerry 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... - Expression of a muscle-specific, nitric oxide synthase transgene prevents muscle membrane injury and reduces muscle inflammation during modified muscle use in miceHal 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... - Shifts in macrophage phenotypes and macrophage competition for arginine metabolism affect the severity of muscle pathology in muscular dystrophyS 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.... - Nitric oxide generated by muscle corrects defects in hippocampal neurogenesis and neural differentiation caused by muscular dystrophyBo 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... - Prednisolone decreases cellular adhesion molecules required for inflammatory cell infiltration in dystrophin-deficient skeletal muscleMichelle 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... - Major basic protein-1 promotes fibrosis of dystrophic muscle and attenuates the cellular immune response in muscular dystrophyMichelle 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.... - Null mutation of myeloperoxidase in mice prevents mechanical activation of neutrophil lysis of muscle cell membranes in vitro and in vivoHal 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... - Cardiomyopathy in dystrophin-deficient hearts is prevented by expression of a neuronal nitric oxide synthase transgene in the myocardiumMichelle 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... - Loss of positive allosteric interactions between neuronal nitric oxide synthase and phosphofructokinase contributes to defects in glycolysis and increased fatigability in muscular dystrophyMichelle 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... - Arginine metabolism by macrophages promotes cardiac and muscle fibrosis in mdx muscular dystrophyMichelle Wehling-Henricks
Department of Integrative Biology and Physiology, University of California Los Angeles, Los Angeles, California, USA
PLoS ONE 5:e10763. 2010.... - Muscleblind-like 2 (Mbnl2) -deficient mice as a model for myotonic dystrophyMinqi 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... - Interplay of IKK/NF-kappaB signaling in macrophages and myofibers promotes muscle degeneration in Duchenne muscular dystrophySwarnali 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... - Interactions between neutrophils and macrophages promote macrophage killing of rat muscle cells in vitroHal X Nguyen
U CA, Los Angeles
J Physiol 547:125-32. 2003.... - Null mutation of gp91phox reduces muscle membrane lysis during muscle inflammation in miceHal X Nguyen
Departments of Physiological Science
J Physiol 553:833-41. 2003.... - Patient survival by Hsp70 membrane phenotype: association with different routes of metastasisKarin 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... - Skipping to new gene therapies for muscular dystrophyJames G Tidball
Nat Med 9:997-8. 2003 - Kinematic modeling of single muscle fiber during diaphragm shorteningBrian 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...
Research Grants
- Myeloid Cell Function in Muscle Injury and RepairJames Tidball; Fiscal Year: 2005..Those findings can indicate new therapeutic approaches to improving muscle function during muscle reloading following periods of reduced loading. ..
- Myeloid Cell Function in Muscular DystrophyJames 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. ..
- Training in Molecular, Cellular & Integrative PhysiologyJames Tidball; Fiscal Year: 2007..abstract_text> ..
- Myeloid Cell Function in Muscle Injury and RepairJames G Tidball; Fiscal Year: 2010..This study will yield the first mechanistic findings concerning macrophage function in muscle repair and growth during increased loading. ..
- Regulation of sarcopenia and muscle dysfunction by nitric oxideJames G Tidball; Fiscal Year: 2010..We anticipate that the results of this investigation can provide new insights into potential therapeutic strategies to reduce sarcopenia. ..
- Regulation of sarcopenia and muscle dysfunction by nitric oxideJames Tidball; Fiscal Year: 2009..We anticipate that the results of this investigation can provide new insights into potential therapeutic strategies to reduce sarcopenia. ..
- REGULATION OF MYOTENDINOUS JUNCTION STRUCTUREJames 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...
- MYOTENDINOUS JUNCTIONS--ADAPTATIONS TO EXERCISEJames Tidball; Fiscal Year: 1991....
- REGULATION OF MYOTENDINOUS JUNCTION STRUCTUREJames 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. ..
- Myeloid Cell Function in Muscle Injury and RepairJames G Tidball; Fiscal Year: 2010..This study will yield the first mechanistic findings concerning macrophage function in muscle repair and growth during increased loading. ..