Metabolic Gene Expression in Fetal and Failing Human Heart

• DOI: 10.1161/hc4901.100526
• Publication Date: 2007-09-28T18:31:09Z
• Authors: Peter Razeghi; Martin E. Young; Joseph L. Alcorn; Christine S. Moravec; O.H. Frazier; Heinrich Taegtmeyer
• Keywords: MYH6; Heart development

Background — Previous studies suggest that the failing heart reactivates fetal genes and reverts to a pattern of energy substrate metabolism. We tested this hypothesis by examining metabolic gene expression profiles in fetal, nonfailing, human heart. Methods Results Human left ventricular tissue (apex) was obtained from 9 10 adult hearts. Using quantitative reverse transcription-polymerase chain reaction, we measured transcript levels atrial natriuretic factor, myosin heavy chain-α -β, 13 key regulators metabolism, which 3 are considered “adult” isoforms (GLUT4, mGS, mCPT-I) “fetal” (GLUT1, lGS, lCPT-I), primarily through previous rodent models. Compared with nonfailing heart, steady-state mRNA factor were increased both The 2 showed highest level Transcript most higher than Adult isogenes predominated all groups always greater induction compared In decreased same as Conclusions exist constitutive inducible forms. profile downregulating transcripts rather upregulating genes.