Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2002-2-11
pubmed:abstractText
Muscle function depends on an adequate ATP supply to sustain the energy consumption associated with Ca(2+) cycling and actomyosin sliding during contraction. In this regulation of energy homeostasis, the creatine kinase (CK) circuit for high energy phosphoryl transfer between ATP and phosphocreatine plays an important role. We earlier established a functional connection between the activity of the CK system and Ca(2+) homeostasis during depolarization and contractile activity of muscle. Here, we show how CK activity is coupled to the kinetics of spontaneous and electrically induced Ca(2+) transients in the sarcoplasm of myotubes. Using the UV ratiometric Ca(2+) probe Indo-1 and video-rate confocal microscopy in CK-proficient and -deficient cultured cells, we found that spontaneous and electrically induced transients were dependent on ryanodine-sensitive Ca(2+) release channels, sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase pumps, extracellular calcium, and functional mitochondria in both cell types. However, at increasing sarcoplasmic Ca(2+) load (induced by electrical stimulation at 0.1, 1, and 10 Hz), the Ca(2+) removal rate and the amount of Ca(2+) released per transient were gradually reduced in CK-deficient (but not wild-type) myotubes. We conclude that the CK/phosphocreatine circuit is essential for efficient delivery of ATP to the sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase pumps and thereby directly influences sarcoplasmic reticulum refilling and the kinetics of the sarcoplasmic Ca(2+) signals.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
277
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5275-84
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:11734556-Adenosine Triphosphate, pubmed-meshheading:11734556-Animals, pubmed-meshheading:11734556-Calcium, pubmed-meshheading:11734556-Calcium-Transporting ATPases, pubmed-meshheading:11734556-Cell Line, pubmed-meshheading:11734556-Creatine Kinase, pubmed-meshheading:11734556-Electrophysiology, pubmed-meshheading:11734556-Kinetics, pubmed-meshheading:11734556-Mice, pubmed-meshheading:11734556-Microscopy, Confocal, pubmed-meshheading:11734556-Muscle, Skeletal, pubmed-meshheading:11734556-Muscles, pubmed-meshheading:11734556-Phosphorylation, pubmed-meshheading:11734556-Potassium Chloride, pubmed-meshheading:11734556-Protein Binding, pubmed-meshheading:11734556-Sarcoplasmic Reticulum, pubmed-meshheading:11734556-Sarcoplasmic Reticulum Calcium-Transporting ATPases, pubmed-meshheading:11734556-Time Factors
pubmed:year
2002
pubmed:articleTitle
The creatine kinase system is essential for optimal refill of the sarcoplasmic reticulum Ca2+ store in skeletal muscle.
pubmed:affiliation
Department of Cell Biology, Nijmegen Center for Molecular Life Sciences, University Medical Center St. Radboud, University of Nijmegen, 6500 HB Nijmegen, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't