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Human eHAND, but not dHAND, is down-regulated in cardiomyopathies
A Natarajan1, H Yamagishi, F Ahmad
1Division of Intensive Care, Department of Pediatrics, University of Texas Southwestern Medical Center, University of Texas Southwestern Medical Center, One Baylor Plaza, Dallas, Texas 75390-9148, USA.
Journal of Molecular and Cellular Cardiology
|September 11, 2001
Summary
Human dHAND and eHAND transcription factors show unique expression patterns in healthy adult hearts. Their downregulation, particularly eHAND, correlates with ischemic and dilated cardiomyopathy progression.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Gene Expression Regulation
Background:
- Fetal gene expression is linked to cardiomyopathy progression.
- Basic helix-loop-helix transcription factors, dHAND and eHAND, are crucial for cardiac development in mice but downregulated in adults.
- Human HAND gene expression in cardiac chambers of healthy and diseased hearts remains uncharacterized.
Purpose of the Study:
- To map human dHAND and eHAND genes to chromosomes.
- To investigate the spatial expression patterns of dHAND and eHAND in healthy human adult cardiac chambers.
- To analyze alterations in dHAND and eHAND expression in human cardiomyopathic hearts.
Main Methods:
- Fluorescent in situ hybridization for gene mapping.
- RNA isolation from four chambers of healthy and cardiomyopathic human hearts.
- Quantitative analysis of dHAND and eHAND gene expression.
Main Results:
- Human dHAND and eHAND genes mapped to chromosomes 4q33 and 5q33.
- dHAND expressed in all four healthy adult chambers, diminished in the right atrium.
- eHAND expressed in ventricles, downregulated in atria; severely downregulated in ischemic and dilated cardiomyopathy.
- dHAND expression remained unchanged across cardiomyopathies.
Conclusions:
- Human dHAND and eHAND exhibit distinct chamber-specific expression patterns in adult hearts.
- Downregulation of eHAND in ischemic and dilated cardiomyopathy suggests a role in disease pathogenesis.
- These findings highlight unique human HAND gene regulation and potential links to heart failure progression.