体内无负荷心脏重现心脏肥大的胎儿基因表达。

Unloaded heart in vivo replicates fetal gene expression of cardiac hypertrophy.

作者信息

Depre C, Shipley G L, Chen W, Han Q, Doenst T, Moore M L, Stepkowski S, Davies P J, Taegtmeyer H

机构信息

Department of Internal Medicine, University of Texas Houston Medical School, 77030, USA.

出版信息

Nat Med. 1998 Nov;4(11):1269-75. doi: 10.1038/3253.

DOI:10.1038/3253

PMID:9809550

Abstract

The cardiac response to increased work includes a reactivation of fetal genes. The response to a decrease in cardiac work is not known. Such information is of clinical interest, because mechanical unloading can improve the functional capacity of the failing heart. We compared here the patterns of gene expression in unloaded rat heart with those in hypertrophied rat heart. Both conditions induced a re-expression of growth factors and proto-oncogenes, and a downregulation of the 'adult' isoforms, but not of the 'fetal' isoforms, of proteins regulating myocardial energetics. Therefore, opposite changes in cardiac workload in vivo induce similar patterns of gene response. Reactivation of fetal genes may underlie the functional improvement of an unloaded failing heart.

摘要

心脏对工作负荷增加的反应包括胎儿基因的重新激活。而心脏工作负荷降低时的反应尚不清楚。这类信息具有临床意义，因为机械卸载可改善衰竭心脏的功能能力。我们在此比较了卸载大鼠心脏与肥大大鼠心脏中的基因表达模式。两种情况均诱导了生长因子和原癌基因的重新表达，以及调节心肌能量代谢的蛋白质的“成人”异构体的下调，但“胎儿”异构体未下调。因此，体内心脏工作负荷的相反变化会诱导相似的基因反应模式。胎儿基因的重新激活可能是卸载衰竭心脏功能改善的基础。