Linked Life Data

15978613

Source:http://linkedlifedata.com/resource/pubmed/id/15978613

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-8-16
pubmed:abstractText
Decreases in total creatine kinase (CK) activity and creatine [Cr] combine to limit the capacity of the failing heart to rapidly re-synthesize ATP (energy reserve). If the loss in energy reserve could be reversed, cardiac contractile reserve may be improved. Here we test whether these changes are reversible during recovery from heart failure. Left ventricular (LV) contractile function was measured in chronically instrumented conscious dogs with heart failure (CHF) induced by cardiac pacing for 3-4 weeks, and after recovery from heart failure (Recovery) (unpaced) for 5-6 weeks. LV contractile function and contractile reserve were depressed in CHF but returned to control in Recovery. CK capacity fell by 55% in CHF due to decreases in [Cr] (-39%) and CK activity (-25%), but was fully restored in Recovery. CK-B isozyme activity, protein (Western) and mRNA levels (real time PCR), respectively, were higher by 2-, 5.4- and 11-fold in CHF and higher by 3-, 2- and 2-fold in Recovery. CK-MM activity was decreased (-30%) in CHF but returned to normal levels during Recovery; CK-M protein was 30% lower in both CHF and Recovery even though there were no changes in mRNA levels. A similar pattern was found for mitochondrial CK (sMtCK). Deceases in CK activity and [Cr] in CHF are reversible. Decreases in CK-MM and sMtCK activities, but not the increases in CK-BB and CK-MB, also reversed. Neither the changes in protein nor mRNA levels for CK-B and CK-M correlated to their activities, suggesting that CK is under complex post-transcriptional regulation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-2828
pubmed:author
pubmed:issnType
Print
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
537-44
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:15978613-Animals, pubmed-meshheading:15978613-Blotting, Western, pubmed-meshheading:15978613-Cardiac Pacing, Artificial, pubmed-meshheading:15978613-Cardiotonic Agents, pubmed-meshheading:15978613-Creatine, pubmed-meshheading:15978613-Creatine Kinase, pubmed-meshheading:15978613-Creatine Kinase, BB Form, pubmed-meshheading:15978613-Creatine Kinase, MM Form, pubmed-meshheading:15978613-Dobutamine, pubmed-meshheading:15978613-Dogs, pubmed-meshheading:15978613-Dose-Response Relationship, Drug, pubmed-meshheading:15978613-Glyceraldehyde-3-Phosphate Dehydrogenases, pubmed-meshheading:15978613-Heart Failure, pubmed-meshheading:15978613-Isoenzymes, pubmed-meshheading:15978613-RNA, Messenger, pubmed-meshheading:15978613-Random Allocation, pubmed-meshheading:15978613-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:15978613-Time Factors
pubmed:year
2005
pubmed:articleTitle
The fall in creatine levels and creatine kinase isozyme changes in the failing heart are reversible: complex post-transcriptional regulation of the components of the CK system.
pubmed:affiliation
Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN 46285, USA. shen_weiqun@lilly.com
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, N.I.H., Extramural