Nuclear magnetic resonance spectroscopy study of muscle growth,mdx dystrophy and glucocorticoid treatments: correlation with repair

McIntosh, Laura; Granberg, Karl-Erik; Briere, K. M.; Anderson, Judy E.

doi:10.1002/(sici)1099-1492(199802)11:1<1::aid-nbm493>3.0.co;2-d

Cited by 75 publications

(67 citation statements)

References 42 publications

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“…The taurine treatment restored MT of exercised dystrophic muscle, in line its high effectiveness when applied in vitro and likely in relation to a direct stimulation of the Ca 2ϩ ATPase pump of sarcoplasmic reticulum (Huxtable, 1992;De Luca et al, 2001). Conditions of muscle taurine depletion are in fact characterized by negative MT and a difficulty of dystrophic muscle to retain adequate amounts of the amino acid has been documented and can be even worsened by exercise (De Luca et al, 1996McIntosh et al, 1998;Matsuzaki et al, 2002). Similarly, PDN was jpet.aspetjournals.org very effective on MT, corresponding to its ability in vitro to decrease cytosolic Ca 2ϩ levels of dystrophic myotubes .…”

Section: Experimental Conditions Drugs In Vitromentioning

confidence: 69%

“…A cellular parameter useful to functionally assess the degeneration and regeneration events occurring in dystrophic fibers is the resting conductance to chloride ions (gCl), the parameter that controls the electrical stability of sarcolemma (Klocke et al, 1994;De Luca et al, 1997). gCl is significantly impaired in progressively degenerating mdx diaphragm (DIA), whereas in the hind limb extensor digitorum longus (EDL) muscle, gCl rises over the control values between the 8th and the 12th week of age, the period of mouse life in which the spontaneous regeneration is still ongoing (De Luca et al, 1997McIntosh et al, 1998). The change in gCl may work as a fine-tuning of the mechanical-stress by modulating sarcolemma excitability (De Luca et al, 1997).…”

mentioning

confidence: 99%

“…The drugs used were creatine, taurine, and insulin-like growth factor-1 (IGF-1). Taurine and creatine levels, normally high in striated fibers, fluctuate in mdx muscle in relation to pathology progression (McIntosh et al, 1998). Creatine stimulates muscle metabolism in vivo, whereas either compounds seem to control calcium-handling mechanisms in vitro, with potential ability to counteract calcium-induced degeneration (Pulido et al, 1998;De Luca et al, 2001).…”

mentioning

confidence: 99%

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Enhanced Dystrophic Progression in mdx Mice by Exercise and Beneficial Effects of Taurine and Insulin-Like Growth Factor-1

Pierno²,

Liantonio³

et al. 2003

J Pharmacol Exp Ther

183

283

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A preclinical screening for prompt-to-use drugs that are safer than steroids and beneficial in Duchenne muscular dystrophy was performed. Compounds able to reduce calcium-induced degeneration (taurine or creatine 10% in chow) or to stimulate regeneration [insulin-like growth factor-1 (IGF-1); 50 or 500 g/kg s.c.] were administered for 4 to 8 weeks to mdx mice undergoing chronic exercise on a treadmill, a protocol to worsen dystrophy progression. ␣-Methyl-prednisolone (PDN; 1 mg/kg) was used as positive control. The effects were evaluated in vivo on forelimb strength and in vitro electrophysiologically on the macroscopic chloride conductance (gCl), an index of degeneration-regeneration events in mdx muscles, and on the mechanical threshold, a calcium-sensitive index of excitation-contraction coupling. The exercise produced a significant weakness and an impairment of gCl, by further decreasing the already low value of degenerating diaphragm (DIA) and fully hampering the increase of gCl typical of regenerating extensor digitorum longus (EDL) mdx muscle. The already negative voltage threshold for contraction of mdx EDL was also slightly worsened. Taurine Ͼ creatine Ͼ IGF-1 counteracted the exercise-induced weakness. The amelioration of gCl was drug-and muscle-specific: taurine was effective in EDL, but not in DIA muscle; IGF-1 and PDN were fully restorative in both muscles, whereas creatine was ineffective. An acute effect of IGF-1 on gCl was observed in vitro in untreated, but not in IGF-1-treated exercised mdx muscles. Taurine Ͼ PDN Ͼ IGF-1, but not creatine, significantly ameliorated the negative threshold voltage values of the EDL fibers. The results predict a potential benefit of taurine and IGF-1 for treating human dystrophy.

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Section: Experimental Conditions Drugs In Vitromentioning

confidence: 69%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Enhanced Dystrophic Progression in mdx Mice by Exercise and Beneficial Effects of Taurine and Insulin-Like Growth Factor-1

Pierno²,

Liantonio³

et al. 2003

J Pharmacol Exp Ther

183

283

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“…These included changes in the lipid components of membranes (Gillet et al, 1993), pH and energy metabolism using proton and phosphorous NMR spectroscopy in muscle (Dunn et al, , 1992Radda, 1999) and/or brain (Rae et al, 1998;Tracey et al, 1996a,b), and treatment responses that were observed in skeletal muscle including the diaphragm, and in cardiac muscle (Anderson et al, 1998McIntosh et al, 1998aMcIntosh et al, ,b,c, 1994Skrabek and Anderson, 2001).…”

Section: A U T H O R ' S P E R S O N a L C O P Ymentioning

confidence: 99%

“…Central myofiber nuclei are apparent only in those parts of muscle fibers that have undergone one or more regenerative events, and CNI is used as an index of accumulated disease progression (Karpati et al, 1988). An early NMR spectroscopy study correlated a number of metabolites including peaks from taurine in a muscle sample, with CNI in sections of the same muscle (McIntosh et al, 1998a). This was an essential step in developing an understanding that metabolite studies by NMR could provide a powerful tool for non-invasive diagnostic studies of muscle pathology and treatment effects.…”

Section: A U T H O R ' S P E R S O N a L C O P Ymentioning

confidence: 99%

Methods and biomarkers for the diagnosis and prognosis of cancer and other diseases: Towards personalized medicine

Anderson

Hansen

Mooren

et al. 2006

Drug Resistance Updates

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The rapid development of new diagnostic procedures, the mapping of the human genome, progress in mapping genetic polymorphisms, and recent advances in nucleic acid-and protein chip technologies are driving the development of personalized therapies. This breakthrough in medicine is expected to be achieved largely due to the implementation of "lab-on-the-chip" technology capable of performing hundreds, even thousands of biochemical, cellular and genetic tests on a single sample of blood or other body fluid. Focusing on a few disease-specific examples, this review discusses selected technologies and their combinations likely to be incorporated in the "lab-on-the-chip" and to provide rapid and versatile information about specific diseases entities. Focusing on breast cancer and after an overview of single-nucleotide polymorphism (SNP)-screening methodologies, we discuss the diagnostic and prognostic importance of SNPs. Next, using Duchenne muscular dystrophy (DMD) as an example, we provide a brief overview of powerful and innovative integration of traditional immuno-histochemistry techniques with advanced biophysical methods such as NMR-spectroscopy or Fourier-transformed infrared (FT-IR) spectroscopy. A brief overview of the challenges and opportunities provided by protein and aptamer microarrays follows. We conclude by highlighting novel and promising biochemical markers for the development of personalized treatment of cancer and other diseases: serum cytochrome c, cytokeratin-18 and -19 and their proteolytic fragments for the detection and quantitation of malignant tumor mass, tumor cell turn-over, inflammatory processes during hepatitis and Epstein-Barr virus (EBV)-induced hemophagocytic lymphohistiocytosis and apoptotic/necrotic cancer cell death.

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Regeneration and myogenic cell proliferation correlate with taurine levels in dystrophin- and MyoD-Deficient muscles

et al. 1998

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This study coupled proton magnetic resonance spectroscopy (1H-NMR) and in situ hybridization plus autoradiography in a novel examination of different phenotypes of adult myogenesis that arise from genetic disruptions in mice. Study of muscle extracts from normal and dystrophin-deficient mdx limb and diaphragm muscles confirmed our previous findings linking taurine and muscle regeneration at the peak of damage and repair. 1H-NMR distinguished biochemical differences in regenerating muscles that were consistent with the extent of repair in three strains: mdx dystrophic mice; MyoD(-/-) mice that lack expression of the early myogenic regulatory gene MyoD; and a double-mutant mdx:MyoD(-/-) strain lacking expression of both MyoD and dystrophin. We tested the hypothesis that differences in spectra according to genotype and the regeneration phenotype are related specifically to proliferation by committed myogenic precursor cells. 1H-NMR distinguished the three mutant strains: Taurine was highest in mdx muscles, with the phenotype of most effective regeneration; lowest in MyoD(-/-) muscles, with the least effective formation of new muscle in repair, as reported previously; and intermediate in double-mutant muscles, now reported to show an intermediate repair phenotype. The early and late muscle precursors (mpcs) expressing myf5 and myogenin were examined for proliferation. Eighteen percent of mdx myf5-positive mpcs were proliferative, whereas myf5-positive mpcs did not proliferate in regenerating muscles that lacked MyoD expression. By contrast, whereas 30% of myogenin-positive mpcs were proliferative in mdx muscles, almost none were proliferative in MyoD(-/-) muscles, and 12% were proliferative in double-mutant muscles. Therefore, the extent of accumulated structural regeneration, taurine levels, and proliferation of late mpc (expressing myogenin) were congruent across genotypes. Proliferation by early mpc (expressing myf5) was inhibited by the lack of MyoD expression during muscle regeneration. These studies indicate the potential for 1H-NMR monitoring of muscle status in disease, regeneration, and treatment.

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Nuclear magnetic resonance spectroscopy study of muscle growth,mdx dystrophy and glucocorticoid treatments: correlation with repair

Cited by 75 publications

References 42 publications

Enhanced Dystrophic Progression in mdx Mice by Exercise and Beneficial Effects of Taurine and Insulin-Like Growth Factor-1

Enhanced Dystrophic Progression in mdx Mice by Exercise and Beneficial Effects of Taurine and Insulin-Like Growth Factor-1

Methods and biomarkers for the diagnosis and prognosis of cancer and other diseases: Towards personalized medicine

Regeneration and myogenic cell proliferation correlate with taurine levels in dystrophin- and MyoD-Deficient muscles

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