Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
1996-10-23
|
| pubmed:abstractText |
After excitation of skeletal muscle, the disturbed ion homeostasis is restored by Na+, K+ ATPase of the sarcolemma and Ca2+ ATPase of the sarcoplasmic reticulum (SR). Contrary to Na+, K+ ATPase, the concentration and isoenzyme distribution of SR Ca2+ ATPase in human skeletal muscle depend on fibre type and age. In cultured human muscle cells the concentration and activity of Na+, K+ ATPase and SR Ca2+ ATPase increase with maturation. In skeletal muscle and cultured muscle cells of patients suffering from myotonic dystrophy (MyD), the activity and the concentration of both Na+, K+ ATPase and SR Ca2+ ATPase are decreased by about 40%. In addition, we measured in cultured MyD muscle cells at rest an increased cytosolic Ca2+ concentration ([Ca2+]i) caused by active voltage-operated Ca2+ channels, which are inactive in resting control cells. However, the restoration of a stimulus-induced Ca2+ transient is unaffected. A differentiation-related disturbance of membranes or a modulation defect of membrane proteins may play a role in MyD. In skeletal muscle and cultured muscle cells of patients suffering from Brody's disease, which is characterized by impaired muscle relaxation, the SR Ca2+ ATPase activity is reduced by about 50%, but the concentrations of total SR Ca2+ ATPase and the predominant SERCA1 isoform are normal. Diseased muscle cells show a delayed restoration of [Ca2+]i after stimulation, which might be explained by structural modifications of SERCA1. Reduction of the Ca2+ release by drugs balances the excitation-relaxation cycle of the pathological cells.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Dantrolene,
http://linkedlifedata.com/resource/pubmed/chemical/Muscle Relaxants, Central,
http://linkedlifedata.com/resource/pubmed/chemical/Nifedipine,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Potassium-Exchanging ATPase,
http://linkedlifedata.com/resource/pubmed/chemical/Verapamil
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0001-6772
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
156
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
355-67
|
| pubmed:dateRevised |
2007-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:8729696-Acetylcholine,
pubmed-meshheading:8729696-Adolescent,
pubmed-meshheading:8729696-Adult,
pubmed-meshheading:8729696-Biological Transport, Active,
pubmed-meshheading:8729696-Calcium,
pubmed-meshheading:8729696-Calcium Channel Blockers,
pubmed-meshheading:8729696-Cells, Cultured,
pubmed-meshheading:8729696-Dantrolene,
pubmed-meshheading:8729696-Female,
pubmed-meshheading:8729696-Homeostasis,
pubmed-meshheading:8729696-Humans,
pubmed-meshheading:8729696-Immunohistochemistry,
pubmed-meshheading:8729696-Male,
pubmed-meshheading:8729696-Middle Aged,
pubmed-meshheading:8729696-Muscle, Skeletal,
pubmed-meshheading:8729696-Muscle Relaxants, Central,
pubmed-meshheading:8729696-Muscular Dystrophies,
pubmed-meshheading:8729696-Nifedipine,
pubmed-meshheading:8729696-Potassium Chloride,
pubmed-meshheading:8729696-Sarcoplasmic Reticulum,
pubmed-meshheading:8729696-Sodium-Potassium-Exchanging ATPase,
pubmed-meshheading:8729696-Verapamil
|
| pubmed:year |
1996
|
| pubmed:articleTitle |
Ion transport in human skeletal muscle cells: disturbances in myotonic dystrophy and Brody's disease.
|
| pubmed:affiliation |
Department of Biochemistry, University of Nijmegen, The Netherlands.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|