[Cardiac gene expression after brief coronary occlusion].
In the pig short coronary occlusions induce molecular damage on the protein level in the myocardium, which elicit repair mechanisms by increased transcription and translation, including the activation of potential transcription factors (protooncogenes), genes involved in repair processes (heat shock genes) or calcium-binding genes. Additionally, some growth factors like insulin-like growth factor II show increased transcription in accordance with their function as trophic factors for reversibly injured myocardium. Changes in mRNA levels mostly are due to increased transcription rates and rarely due to prolonged half-life of the mRNA. However, at present our data do not allow us to conclude which genes are causative for myocardial stunning and/or ischemic preconditioning.
Zimmermann
R
R
Max-Planck-Institut, Abteilung für Experimentelle Kardiologie, Bad Nauheim.
Andres
J
J
Brand
T
T
Frass
O
O
Kluge
A
A
Knöll
R
R
Vogt
A
A
Schaper
W
W
D000818:Animals; D015870:Gene Expression / Q000502:physiology; D006133:Growth Substances / Q000235:genetics*; D006360:Heat-Shock Proteins / Q000235:genetics*; D006801:Humans; D009203:Myocardial Infarction / Q000235:genetics* / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000235:genetics* / Q000473:pathology; D011519:Proto-Oncogenes / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics; D013552:Swine; D014157:Transcription Factors / Q000235:genetics*; D014158:Transcription, Genetic / Q000235:genetics
D006133:Growth Substances; D006360:Heat-Shock Proteins; D012333:RNA, Messenger; D014157:Transcription Factors