Serum parvalbumin, an indicator of muscle disease in murine dystrophy and myotonia

Jockusch, Harald; Friedrich, Gudrun; Zippel, Monika

doi:10.1002/mus.880130613

Cited by 19 publications

(11 citation statements)

References 28 publications

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“…In accord with previous reports, the mdx mice did not show striking alterations in development [1,10], with their mean body weight even being increased compared with control mice at 6-7 months of age [30]. High activities of the muscular enzyme creatine kinase were present in the serum of mdx compared with control mice, as previously described [1,[31][32][33]. This measurement was used in our study to confirm the phenotype of each mouse.…”

Section: Discussionsupporting

confidence: 89%

Expression of the glucose transporter GLUT4 in the muscular dystrophic mdx mouse

Olichon-Berthe

Gautier

Obberghen

et al. 1993

Biochemical Journal

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Glucose transporter protein levels have been investigated in mdx and control (C57Bl/1O) mice. Crude membrane fractions (microsomes plus plasma membranes) were prepared from skeletal muscle, heart, diaphragm and brain of 5-6-week-old and 6-7-month-old control and mdx mice. Using Western blot analysis with C-terminal-specific anti-peptide antibodies, we investigated the glucose transporters GLUT4 in the different muscle tissues and GLUTI in brain. In skeletal tissue from the hindlegs, GLUT4 was increased by -55 % in mdx mice compared with control mice at both ages studied. In the diaphragm, the amount of GLUT4 protein was unchanged in young mdx mice, and was decreased by 37.4 + 4.7% in older mice compared with agematched control mice. No difference was observed between mdx and control mice in the amounts of GLUT4 and GLUTI in heart and brain preparations respectively. To determine whether the change in GLUT4 protein observed in the diaphragm and

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Section: Discussionsupporting

confidence: 89%

Expression of the glucose transporter GLUT4 in the muscular dystrophic mdx mouse

Olichon-Berthe

Gautier

Obberghen

et al. 1993

Biochemical Journal

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“…In addition, findings on the major cytoplasmic Ca 2ϩ binding element parvalbumin in dystrophic fast-twitch fibers (27) suggest that overall Ca 2ϩ handling is reorganized in mdx muscle. The fact that parvalbumin protein expression is not changed in muscular dystrophy (34), but an upregulation of parvalbumin mRNA levels is observed (27) exchanger. Potential abnormalities in these Ca 2ϩ handling components might also play a role in altered ion homeostasis in mdx muscle fibers.…”

Section: Discussionmentioning

confidence: 89%

Drastic reduction of calsequestrin-like proteins and impaired calcium binding in dystrophicmdxmuscle

Culligan

Banville

Dowling

et al. 2002

Journal of Applied Physiology

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Although the reduction in dystrophin-associated glycoproteins is the primary pathophysiological consequence of the deficiency in dystrophin, little is known about the secondary abnormalities leading to x-linked muscular dystrophy. As abnormal Ca2+ handling may be involved in myonecrosis, we investigated the fate of key Ca2+ regulatory membrane proteins in dystrophic mdx skeletal muscle membranes. Whereas the expression of the ryanodine receptor, the dihydropyridine receptor, the Ca2+-ATPase, and calsequestrin was not affected, a drastic decline in calsequestrin-like proteins of 150–220 kDa was observed in dystrophic microsomes using one-dimensional immunoblotting, two-dimensional immunoblotting with isoelectric focusing, diagonal two-dimensional blotting technique, and immunoprecipitation. In analogy, overall Ca2+ binding was reduced in the sarcoplasmic reticulum of dystrophic muscle. The reduction in Ca2+ binding proteins might be directly involved in triggering impaired Ca2+ sequestration within the lumen of the sarcoplasmic reticulum. Thus disturbed sarcolemmal Ca2+ fluxes seem to influence overall Ca2+homeostasis, resulting in distinct changes in the expression profile of a subset of Ca2+ handling proteins, which might be an important factor in the progressive functional decline of dystrophic muscle fibers.

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“…Creatine kinase protein is used not only as a diagnosis of brain energetic value as mentioned above, but also of diseases like cardiac infarction and skeletal muscle necrosis [50]. In muscle, creatine kinase is specifically bound to sarcoendoplasmic reticulum, and regulates calcium uptake and ATP/ADP ratios [51], thus is directly involved in muscle contraction.…”

Section: Resultsmentioning

confidence: 99%

Linking mechanistic and behavioral responses to sublethal esfenvalerate exposure in the endangered delta smelt; Hypomesus transpacificus (Fam. Osmeridae)

et al. 2009

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BackgroundThe delta smelt (Hypomesus transpacificus) is a pelagic fish species listed as endangered under both the USA Federal and Californian State Endangered Species Acts and considered an indicator of ecosystem health in its habitat range, which is limited to the Sacramento-San Joaquin estuary in California, USA. Anthropogenic contaminants are one of multiple stressors affecting this system, and among them, current-use insecticides are of major concern. Interrogative tools are required to successfully monitor effects of contaminants on the delta smelt, and to research potential causes of population decline in this species. We have created a microarray to investigate genome-wide effects of potentially causative stressors, and applied this tool to assess effects of the pyrethroid insecticide esfenvalerate on larval delta smelt. Selected genes were further investigated as molecular biomarkers using quantitative PCR analyses.ResultsExposure to esfenvalerate affected swimming behavior of larval delta smelt at concentrations as low as 0.0625 μg.L-1, and significant differences in expression were measured in genes involved in neuromuscular activity. Alterations in the expression of genes associated with immune responses, along with apoptosis, redox, osmotic stress, detoxification, and growth and development appear to have been invoked by esfenvalerate exposure. Swimming impairment correlated significantly with expression of aspartoacylase (ASPA), an enzyme involved in brain cell function and associated with numerous human diseases. Selected genes were investigated for their use as molecular biomarkers, and strong links were determined between measured downregulation in ASPA and observed behavioral responses in fish exposed to environmentally relevant pyrethroid concentrations.ConclusionsThe results of this study show that microarray technology is a useful approach in screening for, and generation of molecular biomarkers in endangered, non-model organisms, identifying specific genes that can be directly linked with sublethal toxicological endpoints; such as changes in expression levels of neuromuscular genes resulting in measurable swimming impairments. The developed microarrays were successfully applied on larval fish exposed to esfenvalerate, a known contaminant of the Sacramento-San Joaquin estuary, and has permitted the identification of specific biomarkers which could provide insight into the factors contributing to delta smelt population decline.

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Serum parvalbumin, an indicator of muscle disease in murine dystrophy and myotonia

Cited by 19 publications

References 28 publications

Expression of the glucose transporter GLUT4 in the muscular dystrophic mdx mouse

Expression of the glucose transporter GLUT4 in the muscular dystrophic mdx mouse

Drastic reduction of calsequestrin-like proteins and impaired calcium binding in dystrophicmdxmuscle

Linking mechanistic and behavioral responses to sublethal esfenvalerate exposure in the endangered delta smelt; Hypomesus transpacificus (Fam. Osmeridae)

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