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Published on: January 18, 2019
Gene expression pattern in biomechanically stretched cardiomyocytes: evidence for a stretch-specific gene program.
Derk Frank1, Christian Kuhn, Benedikt Brors
1Department of Internal Medicine III, University of Heidelberg, Heidelberg, Germany.
Hypertension (Dallas, Tex. : 1979)
|December 26, 2007
Summary
Mechanical stress on heart cells causes cardiac hypertrophy. This study reveals a unique gene expression program activated by stretch, partly mediated by angiotensin II signaling, offering new insights into heart failure mechanisms.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Cellular Mechanotransduction
Background:
- Biomechanical stress, such as pressure overload, is a known trigger for cardiac hypertrophy, a precursor to heart failure.
- The precise molecular mechanisms by which mechanical stress is sensed and transduced in cardiomyocytes remain incompletely understood.
Purpose of the Study:
- To systematically identify and characterize the signal transduction pathways involved in cardiomyocyte response to mechanical stress.
- To compare the gene expression profiles of cardiomyocytes under mechanical stretch versus pharmacological stimulation to uncover stretch-specific responses.
Main Methods:
- Genome-wide gene expression analysis using microarrays on neonatal rat ventricular cardiomyocytes subjected to biaxial stretch or phenylephrine (PE) stimulation.
- Confirmation of differential gene expression using real-time polymerase chain reaction (RT-PCR).
- Validation of specific protein level changes for key genes.
Main Results:
- Microarray analysis identified 164 upregulated and 21 downregulated genes (>2.0-fold and <0.5-fold, respectively) in response to stretch (P<0.01).
- Both stretch and PE induced fetal gene program markers (e.g., BNP). Known stretch-responsive genes (HSP70, c-myc) were upregulated.
- Stretch preferentially induced cardioprotective genes GDF15 and Hmox1, which were also upregulated by angiotensin II and inhibited by an AT(1) receptor blocker, suggesting angiotensin II-dependent signaling.
Conclusions:
- A comprehensive gene expression profile for cardiomyocytes under biomechanical stress was established, distinct from pharmacologically induced hypertrophy.
- A stretch-specific gene program exists in cardiomyocytes.
- Angiotensin II-dependent signaling pathways play a significant role in mediating the biomechanical induction of specific genes like GDF15 and Hmox1.
