Research Topics
| D G AllenSummaryAffiliation: University of Sydney Country: Australia Publications
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Detail Information
Publications
Calcium and the damage pathways in muscular dystrophyDavid G Allen
School of Medical Sciences and Bosch Institute, University of Sydney F13, NSW 2006, Australia
Can J Physiol Pharmacol 88:83-91. 2010..Activity of this kinase causes opening of SACNSC and allows Ca2+ entry. This pathway appears to be a significant cause of muscle damage in DMD...
Physiology. Lactic acid--the latest performance-enhancing drugDavid Allen
Institute of Biomedical Research, University of Sydney, NSW 2006, Australia
Science 305:1112-3. 2004- Intracellular ATP measured with luciferin/luciferase in isolated single mouse skeletal muscle fibresDavid G Allen
Department of Physiology, University of Sydney F13, NSW 2006, Australia
Pflugers Arch 443:836-42. 2002..A depletion of global [ATP](i) is not observed in all fatiguing fibres and cannot be the sole cause of the final phase of fatigue... - Impaired calcium release during fatigueD G Allen
School of Medical Sciences and Bosch Institute, Univ of Sydney F13, NSW 2006, Australia
J Appl Physiol 104:296-305. 2008..Further progress requires the development of methods that can identify impaired SR Ca(2+) release in intact, blood-perfused muscles and that can distinguish between the various mechanisms proposed... - Skeletal muscle function: role of ionic changes in fatigue, damage and diseaseD G Allen
School of Biomedical Sciences and Institute for Biomedical Research, University of Sydney, Sydney, New South Wales, Australia
Clin Exp Pharmacol Physiol 31:485-93. 2004..Currently, we are testing whether blockers of the stretch-activated channels given systemically to mdx mice can protect against some features of the disease... 
Role of phosphate and calcium stores in muscle fatigueD G Allen
Department of Physiology and Institute of Biomedical Research, University of Sydney F13, NSW 2006, Australia
J Physiol 536:657-65. 2001..The relevance of this mechanism in different types of fatigue in humans is considered...- Role of the cardiac Na+/H+ exchanger during ischemia and reperfusionDavid G Allen
Department of Physiology and Institute for Biomedical Research, University of Sydney F13, NSW 2006, Sydney, Australia
Cardiovasc Res 57:934-41. 2003..This issue is central to the design of a clinical trial of NHE1 inhibitors in the treatment of human cardiac ischemia and the existing clinical trials are considered in this light... - Understanding muscle from its lengthD G Allen
School of Medical Sciences and Bosch Institute, University of Sydney, NSW, Australia
J Physiol 583:3-4. 2007 - Activity of the Na+/H+ exchanger contributes to cardiac damage following ischaemia and reperfusionD G Allen
Institute for Biomedical Research, Department of Physiology, University, of Sydney, New South Wales, Australia
Clin Exp Pharmacol Physiol 27:727-33. 2000..The intracellular regulation of the Na+/H+ exchanger appears to be an important component of these pathways and may become a focus for therapeutic approaches... - Why stretched muscles hurt--is there a role for half-sarcomere dynamics?David G Allen
School of Medical Sciences, University of Sydney, NSW 2006, Australia
J Physiol 573:4. 2006 - The role of ATP in the regulation of intracellular Ca2+ release in single fibres of mouse skeletal muscleD G Allen
Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden
J Physiol 498:587-600. 1997..These observations suggest that site(s) which either bind ATP or depend on ATP hydrolysis have a key role in excitation-contraction coupling and in muscle fatigue... - Mechanisms of stretch-induced muscle damage in normal and dystrophic muscle: role of ionic changesD G Allen
School of Medical Sciences, University of Sydney, NSW, Australia
J Physiol 567:723-35. 2005..A hypothetical scheme for muscle damage which incorporates these ideas is presented... - Skeletal muscle fatigue: cellular mechanismsD G Allen
School of Medical Sciences and Bosch Institute, University of Sydney, Sydney, New South Wales, Australia
Physiol Rev 88:287-332. 2008.... - Functional significance of Ca2+ in long-lasting fatigue of skeletal muscleH Westerblad
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
Eur J Appl Physiol 83:166-74. 2000..We will also discuss the relationship between gross morphological changes in muscle fibres and long-lasting failure of SR Ca2+ release. Finally, a model linking muscle cell dysfunction and muscle pain is proposed... - Slowed relaxation in fatigued skeletal muscle fibers of Xenopus and Mouse. Contribution of [Ca2+]i and cross-bridgesH Westerblad
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
J Gen Physiol 109:385-99. 1997..In conclusion, slowing of relaxation in fatigued Xenopus fibers is caused by impaired Ca2+ handling and altered cross-bridge kinetics, whereas the slowing in mouse fibers is only due to altered cross-bridge kinetics... - Activation of Ca(2+)-dependent protein kinase II during repeated contractions in single muscle fibres from mouse is dependent on the frequency of sarcoplasmic reticulum Ca(2+) releaseJ Aydin
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
Acta Physiol (Oxf) 191:131-7. 2007..To investigate the importance and contribution of calmodulin-dependent protein kinase II (CaMKII) activity on sarcoplasmic reticulum (SR) Ca(2+)-release in response to different work intensities in single, intact muscle fibres... - Streptomycin reduces stretch-induced membrane permeability in muscles from mdx miceNicholas P Whitehead
School of Medical Sciences and Institute for Biomedical Research, University of Sydney F13, Sydney, NSW, Australia
Neuromuscul Disord 16:845-54. 2006..The results suggest that Ca(2+) entry through SACs activates Ca(2+) -dependent pathways, which are the main cause of the increased membrane permeability in mdx muscle... - The role of reactive oxygen species in the hearts of dystrophin-deficient mdx miceIwan A Williams
Bosch Institute, School of Medical Sciences, University of Sydney F13, NSW 2006 Australia
Am J Physiol Heart Circ Physiol 293:H1969-77. 2007..Therapies designed to reduce oxidative damage might be beneficial to DMD patients with heart failure... - The use of the indicator fluo-5N to measure sarcoplasmic reticulum calcium in single muscle fibres of the cane toadA A Kabbara
Department of Physiology and Institute of Biomedical Research, University of Sydney F13, NSW 2006, Australia
J Physiol 534:87-97. 2001..This reduction in [Ca(2+)](SR) will contribute to the failure of Ca(2+) delivery to the myofilaments which is an important cause of muscle fatigue... - Interactions between intracellular calcium and phosphate in intact mouse muscle during fatigueD G Allen
School of Medical Sciences and Bosch Institute, University of Sydney, Sydney, NSW 2006, Australia
J Appl Physiol 111:358-66. 2011..We suggest that both changes contribute to the fatigue. A likely cause of the decline in tetanic myoplasmic Ca(2+) is precipitation of CaP(i) in the SR... - C2C12 co-culture on a fibroblast substratum enables sustained survival of contractile, highly differentiated myotubes with peripheral nuclei and adult fast myosin expressionS T Cooper
Institute for Neuromuscular Research, The Children s Hospital at Westmead, Sydney, Australia
Cell Motil Cytoskeleton 58:200-11. 2004.... - Intracellular calcium handling in ventricular myocytes from mdx miceIwan A Williams
Bosch Institute, School of Medical Sciences, University of Sydney F13, NSW 2006 Australia
Am J Physiol Heart Circ Physiol 292:H846-55. 2007..Early in the disease process and before the onset of clinical symptoms increased, SAC activity may underlie the abnormal Ca(2+) handling in young mdx mice... - Fibroblasts modulate cardiomyocyte excitability: implications for cardiac gene therapyE Kizana
Department of Cardiology, Westmead Hospital, Westmead, New South Wales, Australia
Gene Ther 13:1611-5. 2006..Expression of Cx43 in fibroblasts from Cx43 knockout mice restored cardiomyocyte beat frequency, to rates comparable with those observed in co-culture with WT fibroblasts... - Intracellular calibration of the calcium indicator indo-1 in isolated fibers of Xenopus muscleH Westerblad
Department of Physiology, University of Sydney, Australia
Biophys J 71:908-17. 1996..This makes indo-1 less suitable for measurements of [Ca2+]i during twitches, whereas it is fast enough to follow most aspects of [Ca2+]i during tetani, including the relaxation phase... - Does Ca2+ release from the sarcoplasmic reticulum influence heart rate?Y K Ju
Department of Physiology and Institute for Biomedical Research, University of Sydney F13, Sydney, New South Wales 2006, Australia
Clin Exp Pharmacol Physiol 28:703-8. 2001..5. These studies show that Ca2+ handling by the pacemaker cells makes an important contribution to the regulation of pacemaker activity... - Eccentric muscle damage: mechanisms of early reduction of forceD G Allen
Department of Physiology and Institute for Biomedical Research, University of Sydney, Australia
Acta Physiol Scand 171:311-9. 2001..The potential of these mechanisms to contribute to the effects of muscle training and to the symptoms of muscle disease, such as muscular dystrophy, is considered... - Effects of stretch-activated channel blockers on [Ca2+]i and muscle damage in the mdx mouseElla W Yeung
School of Medical Sciences and Institute for Biomedical Research, University of Sydney F13, NSW 2006, Australia
J Physiol 562:367-80. 2005..This result suggests that blockers of stretch-activated channels may protect against muscle damage in the intact mdx mouse... - Reactive oxygen species reduce myofibrillar Ca2+ sensitivity in fatiguing mouse skeletal muscle at 37 degrees CTerence R Moopanar
Institute for Biomedical Sciences, School of Medical Sciences, University of Sydney F13, NSW 2006, Australia
J Physiol 564:189-99. 2005..This study confirms the importance of ROS in fatigue at 37 degrees C and shows that the mechanism of action of ROS is a decline in myofibrillar Ca2+ sensitivity... - The activity-induced reduction of myofibrillar Ca2+ sensitivity in mouse skeletal muscle is reversed by dithiothreitolTerence R Moopanar
Institute for Biomedical Sciences, School of Medical Sciences, University of Sydney F13, NSW 2006, Australia
J Physiol 571:191-200. 2006..We propose that critical sulphydryl groups on the target protein(s) are converted to disulphide bonds and this reaction reduces Ca2+ sensitivity... - Cellular mechanisms of skeletal muscle fatigueHakan Westerblad
Department of Physiology and Pharmacology, Karolinska Instituet, SE 171 77 Stockholm, Sweden
Adv Exp Med Biol 538:563-70; discussion 571. 2003 - Gadolinium reduces short-term stretch-induced muscle damage in isolated mdx mouse muscle fibresElla W Yeung
Institute for Biomedical Research and Department of Physiology, University of Sydney F13, NSW 2006, Australia
J Physiol 552:449-58. 2003..These experiments show that part of the short-term damage caused by stretch in mdx fibres can be prevented by blocking stretch-activated channels... - Store-operated Ca2+ entry and TRPC expression; possible roles in cardiac pacemaker tissueYue Kun Ju
School of Medical Sciences F13, University of Sydney, Sydney, NSW 2006, Australia
Heart Lung Circ 16:349-55. 2007..Many hormones, drugs and interventions such as ischaemia and stretch, which alter Ca(2+) handling, will also modulate pacemaker firing thought their effect on SOCCs... - TRPC1 binds to caveolin-3 and is regulated by Src kinase - role in Duchenne muscular dystrophyOthon L Gervasio
School of Medical Sciences, Discipline of Physiology F13, Bosch Institute, The University of Sydney, NSW 2006, Australia
J Cell Sci 121:2246-55. 2008..Because ROS production is increased in mdx/DMD, these results suggest that a ROS-Src-TRPC1/caveolin-3 pathway contributes to the pathogenesis of mdx/DMD... - Store-operated Ca2+ influx and expression of TRPC genes in mouse sinoatrial nodeYue Kun Ju
School of Medical Sciences and Bosch Institute, University of Sydney, Sydney, NSW, Australia
Circ Res 100:1605-14. 2007..These results indicate that mouse SAN exhibits store-operated Ca(2+) activity which may be attributable to TRPC expression, and suggest that SOCCs may be involved in regulating pacemaker firing rate... - Stretch-induced membrane damage in muscle: comparison of wild-type and mdx miceDavid G Allen
Bosch Institute and School of Medical Sciences, University of Sydney, F13, Sydney, NSW, 2006, Australia
Adv Exp Med Biol 682:297-313. 2010..Instead we review the substantial evidence that the membrane permeability is a secondary consequence of the mechanical events in which elevated intracellular calcium and reactive oxygen species are important intermediaries... - N-Acetylcysteine ameliorates skeletal muscle pathophysiology in mdx miceNicholas P Whitehead
Bosch Institute, School of Medical Sciences, University of Sydney F13, Sydney, NSW 2006, Australia
J Physiol 586:2003-14. 2008..These results offer the prospect that antioxidants such as NAC could have therapeutic potential for DMD patients... - Cyanide inhibits the Na+/Ca2+ exchanger in isolated cardiac pacemaker cells of the cane toadYue-kun Ju
Department of Physiology, Institute for Biomedical Research, University of Sydney, F13, Sydney, NSW, Australia
Pflugers Arch 449:442-8. 2005..These results show that cyanide (CN-) inhibits NCX activity at least partly through changes in the intrinsic properties of NCX. The inhibition of NCX probably contributes to the slower firing rate of pacemaker cells in CN-... - Muscle fatigue: the role of intracellular calcium storesDavid G Allen
Department of Physiology, University of Sydney F13, NSW 2006, Australia
Can J Appl Physiol 27:83-96. 2002..This proposes that if phosphate in the myoplasm rises, it enters the SR and binds to Ca2+ as Ca2+ phosphate. The resultant reduction in free Ca2+ within the SR contributes to the reduced Ca2+ release during fatigue... - Early effects of metabolic inhibition on intracellular Ca2+ in toad pacemaker cells: involvement of Ca2+ storesYue-kun Ju
Department of Physiology and Institute for Biomedical Research, University of Sydney, New South Wales 2006, Australia
Am J Physiol Heart Circ Physiol 284:H1087-94. 2003..In conclusion, CN(-) appears to reduce Ca(2+) release from the SR mainly by reducing SR Ca(2+) content. A likely cause of the decreased SR content is reduced Ca(2+) uptake by the SR pump... - Calmodulin kinase modulates Ca2+ release in mouse skeletal musclePasi Tavi
Department of Physiology and Pharmacology, Karolinska Institutet, 171 77 Stockholm, Sweden
J Physiol 551:5-12. 2003..In conclusion, CaMKII-induced phosphorylation facilitates SR Ca2+ release in the basal state and during repeated contractions, providing a positive feedback between [Ca2+]i and SR Ca2+ release... - Muscle damage in mdx (dystrophic) mice: role of calcium and reactive oxygen speciesNicholas P Whitehead
School of Medical Sciences, University of Sydney, Sydney, New South Wales, Australia
Clin Exp Pharmacol Physiol 33:657-62. 2006..There is recent evidence that increased ROS may be important in both the activation of and the damage caused by this inflammatory pathway in mdx muscle... - ATP modulates intracellular Ca2+ and firing rate through a P2Y1 purinoceptor in cane toad pacemaker cellsYue-kun Ju
Department of Physiology, Institute for Biomedical Research, University of Sydney, NSW, Australia
J Physiol 552:777-87. 2003..Our study shows that in toad pacemaker cells, the biphasic effects of ATP on pacemaker activity are mainly through P2Y1 purinoceptors, which are able to modulate Ca2+ release from the SR Ca2+ store... - IGF-1 enhances a store-operated Ca2+ channel in skeletal muscle myoblasts: involvement of a CD20-like proteinYue-kun Ju
Department of Physiology, University of Sydney, NSW, Australia
J Cell Physiol 197:53-60. 2003..However, the SOCC activity observed in C2C12 myoblasts is mediated not by CD20, but by a CD20-like protein. Activation of this SOCC may contribute to IGF-1-induced hypertrophy in these cells... - Iron injections in mice increase skeletal muscle iron content, induce oxidative stress and reduce exercise performanceTrent F Reardon
School of Medical Sciences, Bosch Institute, The University of Sydney, NSW 2006, Australia
Exp Physiol 94:720-30. 2009..In summary, iron accumulation in skeletal muscle may play a significant role in the reduced exercise capacity seen in iron overload disorders and in ageing, and may play an underlying role in skeletal muscle atrophy... - Recent advances in the understanding of skeletal muscle fatigueHakan Westerblad
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
Curr Opin Rheumatol 14:648-52. 2002..The initial defect induced by eccentric contractions is overstretched sarcomeres, but these appear to cause localized membrane tears that subsequently contribute to muscle weakness and damage... - Time to fatigue is increased in mouse muscle at 37 degrees C; the role of iron and reactive oxygen speciesTrent F Reardon
School of Medical Sciences, Bosch Institute, Anderson Stuart Bldg F13, The University of Sydney, NSW 2006, Australia
J Physiol 587:4705-16. 2009..An increase in muscle iron can accelerate ROS production, which may be important during or following exercise and in haemochromatosis, disuse atrophy and sarcopenia... - Skeletal muscle hypertrophy is mediated by a Ca2+-dependent calcineurin signalling pathwayC Semsarian
Victor Chang Cardiac Research Institute, St Vincent s Hospital, New South Wales, Australia
Nature 400:576-81. 1999..We propose that growth-factor-induced skeletal-muscle hypertrophy and changes in myofibre phenotype are mediated by calcium mobilization and are critically regulated by the calcineurin/NF-ATc1 signalling pathway... - Tetraethylammonium blocks muscarinically evoked secretion in the sheep parotid gland by a mechanism additional to its blockade of BK channelsD I Cook
Department of Physiology, University of Sydney, NSW, Australia
Pflugers Arch 420:167-71. 1992.... - Muscle fatigue: lactic acid or inorganic phosphate the major cause?Hakan Westerblad
Department of Physiology and Pharmacology, Karolinska Institutet, SE 171 77 Stockholm, Sweden
News Physiol Sci 17:17-21. 2002..Instead, inorganic phosphate, which increases during fatigue due to breakdown of creatine phosphate, appears to be a major cause of muscle fatigue... - The cardioprotective effects of Na+/H+ exchange inhibition and mitochondrial KATP channel activation are additive in the isolated rat heartXiao-Hui Xiao
Department of Physiology and Institute for Biomedical Research, University of Sydney F13, NSW 2006, Australia
Pflugers Arch 447:272-9. 2003..The combination of these drugs is also highly effective when given 2 min before the end of ischemia... - AICAR inhibits the Na+/H+ exchanger in rat hearts--possible contribution to cardioprotectionTerence R Moopanar
Department of Physiology and Institute for Biomedical Research, University of Sydney, Sydney, NSW 2006, Australia
Pflugers Arch 453:147-56. 2006..We conclude that AICAR inhibits NHE1 through an unidentified pathway. This inhibition may make a contribution to the cardioprotective effects of AICAR... - The role of endogenous angiotensin II in ischaemia, reperfusion and preconditioning of the isolated rat heartXiao-Hui Xiao
Department of Physiology, University of Sydney F13, Sydney, NSW 2006, Australia
Pflugers Arch 445:643-50. 2003..These studies suggest that AII contributes to the activation of NHE1 in early reperfusion and that part of the beneficial effect of preconditioning may be attributed to the abolition of AII-induced activation of NHE1... - The rise of [Na(+)] (i) during ischemia and reperfusion in the rat heart-underlying mechanismsIwan A Williams
Bosch Institute and School of Medical Sciences, University of Sydney, F13 Sydney, NSW 2006, Australia
Pflugers Arch 454:903-12. 2007..The fact that a low concentration of TTX eliminated the rise of [Na(+)](i) during ischemia suggests that I (Na,P) is a major source of Na(+) influx in this model of ischemia... - Development of T-tubular vacuoles in eccentrically damaged mouse muscle fibresElla W Yeung
Department of Rehabilitation Sciences, Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong
J Physiol 540:581-92. 2002..The damage to the T-tubules may underlie a number of the functional changes that occur in eccentrically damaged muscle fibres... - Intracellular sodium in mammalian muscle fibers after eccentric contractionsElla W Yeung
Department of Rehabilitation Sciences, Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong, China
J Appl Physiol 94:2475-82. 2003..These data suggest that Na(+) entry after eccentric contractions may occur principally through stretch-sensitive channels... - Role of the calcium-calpain pathway in cytoskeletal damage after eccentric contractionsBao Ting Zhang
Muscle Physiology Laboratory, Department of Rehabilitation Sciences, Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong
J Appl Physiol 105:352-7. 2008..These results suggest that the cytoskeletal damage and membrane disruption were mediated primarily by increased Ca(2+) influx into muscle cells and subsequent activation of calpain... - Stretch-activated channels in stretch-induced muscle damage: role in muscular dystrophyElla W Yeung
Department of Rehabilitation Sciences, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong, China
Clin Exp Pharmacol Physiol 31:551-6. 2004..Although changes in Na+ accompany stretch-induced muscle injury, we believe that changes in Ca2+ probably have a more central role in the damage process... - Stretch-activated channels in the heart: contributions to length-dependence and to cardiomyopathyMarie Louise Ward
Department of Physiology, Faculty of Medicine and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand
Prog Biophys Mol Biol 97:232-49. 2008..Expression of TRPC1 was increased in the older mdx animals, which have developed a dilated cardiomyopathy, and might therefore contribute to the dilated cardiomyopathy... - Fibroblasts can be genetically modified to produce excitable cells capable of electrical couplingEddy Kizana
Department of Cardiology, Westmead Hospital, Westmead, Australia
Circulation 111:394-8. 2005..CONCLUSIONS: Fibroblasts can be genetically modified to produce excitable cells capable of electrical coupling. These observations strengthen the prospect of developing gene-based strategies for repairing cardiac conduction defects... - Molecular insights from a novel cardiac troponin I mouse model of familial hypertrophic cardiomyopathyTatiana Tsoutsman
Agnes Ginges Centre for Molecular Cardiology, Centenary Institute, Locked Bag 6, Newtown NSW 2042 Australia
J Mol Cell Cardiol 41:623-32. 2006..The cTnI-G203S mutation disrupts interactions with partner proteins, and results in intracellular Ca2+ dysregulation early in life, suggesting a pathogenic role in development of FHC...