[The overexpression of NCAM (CD56) in human hearts is specific for ischemic damage].
The main reason for myocardial dysfunction is chronical myocardial ischemia. Recently we could show, that NCAM (CD56), a neural cell adhesion molecule and member of the immunoglobuline superfamily, and the transcription factor AML1 (RUNX1) are overexpressed in chronic ischemic human heart failure compaired to normal hearts. Here we demonstrate, that the overexpression of NCAM (CD56) is specific for ischemic damage as compaired to other heart diseases including congestive cardiomyopathy, hypertrophic obstrutive cardiomyopathy, myocarditis and sarcoidosis. Concerning the transcriptional regulation of NCAM (CD56) by AML1 (RUNX1) we isolated 3 novel isoforms of AML 1 (RUNX1) with different transactivating function, that might be a regulatory element of the NCAM (CD56) overexpression in chronical myocardial ischemia.
Gattenlöner
S
S
Institut für Pathologie der Universitat Würzburg, Würzburg, Germany.
Waller
C
C
Ertl
G
G
Bültmann
B D
BD
Müller-Hermelink
H K
HK
Marx
A
A
D000328:Adult; D000368:Aged; D019002:CD56 Antigen / Q000235:genetics*; D002648:Child; D050676:Core Binding Factor Alpha 2 Subunit / Q000235:genetics; D005260:Female; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000235:genetics / Q000473:pathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000235:genetics* / Q000473:pathology*; D014157:Transcription Factors / Q000235:genetics
D019002:CD56 Antigen; D050676:Core Binding Factor Alpha 2 Subunit; D014157:Transcription Factors