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Updated: Jun 12, 2026
Single Cell Transcriptional Profiling of Adult Mouse Cardiomyocytes
Published on: December 28, 2011
A gene expression profile of the myocardial response to clenbuterol
Enrique Lara-Pezzi1, Cesare M N Terracciano, Gopal K R Soppa
1Harefield Heart Science Centre, National Heart and Lung Institute, Imperial College, Hill End Road, Harefield, Middlesex, UB9 6JH, UK.
Abstract:
Clenbuterol is currently being used as part of a clinical trial into a novel therapeutic approach for the treatment of end-stage heart failure. The purpose of this study was to determine the global pattern of myocardial gene expression in response to clenbuterol and to identify novel targets and pathways involved. Rats were treated with clenbuterol (n = 6) or saline (n = 6) for periods of 1, 3, 9, or 28 days. Rats treated for 28 days were also subject to continuous electrocardiogram analysis using implantable telemetry. RNA was extracted from rats at days 1 and 28 and used from microarray analysis, and further samples from rats at days 1, 3, 9, and 28 were used for analysis by real-time polymerase chain reaction. Clenbuterol treatment induced rapid development of cardiac hypertrophy with increased muscle mass at day 1 and elevated heart rate and QT interval throughout the 28-day period. Microarray analysis revealed a marked but largely transitory change in gene expression with 1,423 genes up-regulated and 964 genes down-regulated at day 1. Up-regulated genes revealed an unexpected association with angiogenesis and integrin-mediated cell adhesion and signaling. Moreover, direct treatment of endothelial cells cultured in vitro resulted in increased cell proliferation and tube formation. Our data show that clenbuterol treatment is associated with rapid cardiac hypertrophy and identify angiogenesis and integrin signaling as novel pathways of clenbuterol action. The data have implications both for our understanding of the physiologic hypertrophy induced by clenbuterol and for treatment of heart failure.
Insights
Clenbuterol rapidly causes cardiac hypertrophy, affecting gene expression and heart function in rats. This study reveals novel pathways involving angiogenesis and integrin signaling, offering insights into heart failure treatment.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Pharmacology
Background:
- Clenbuterol is under investigation for treating end-stage heart failure.
- Understanding its effects on myocardial gene expression is crucial for therapeutic development.
Purpose of the Study:
- To investigate the global myocardial gene expression patterns induced by clenbuterol.
- To identify novel molecular targets and signaling pathways affected by clenbuterol treatment.
Main Methods:
- Rats were administered clenbuterol or saline and analyzed at multiple time points (1, 3, 9, 28 days).
- Gene expression was assessed using microarray analysis and real-time polymerase chain reaction.
- Electrocardiogram analysis was performed using implantable telemetry.
Main Results:
- Clenbuterol induced rapid cardiac hypertrophy, increased heart rate, and prolonged QT interval.
- Microarray analysis showed significant, albeit transient, changes in gene expression, with numerous genes up-regulated and down-regulated.
- Up-regulated genes were unexpectedly linked to angiogenesis and integrin signaling pathways.
- In vitro studies demonstrated increased endothelial cell proliferation and tube formation upon clenbuterol treatment.
Conclusions:
- Clenbuterol treatment is associated with swift cardiac hypertrophy.
- Angiogenesis and integrin signaling represent novel pathways mediating clenbuterol's action.
- Findings provide insights into physiological hypertrophy and potential heart failure therapeutic strategies.
