April 1, 2007The FASEB Journal
MicroRNAs are aberrantly expressed in hypertrophic heart: do they play a role in cardiac hypertrophy?
Key result
Antisense depletion of miR-21 reduces cardiomyocyte hypertrophy in a mouse model of aortic banding.
- P<0.01
Why the study?
The roles of miRNAs in heart diseases, including cardiac hypertrophy, were completely unknown despite their high expression in the heart.
Population
Hypertrophic mouse hearts after aortic banding and cultured neonatal hypertrophic cardiomyocytes
Comparison
Aortic banding vs sham surgical group; miR-21 knockdown vs control in cardiomyocytes
Design
Preclinical experimental study with microarray and molecular analyses
Follow-up
Up to 21 days after aortic banding
Authors
Discussion
Loading...
Member takes
Implication
Hypothesis-generating for miRNA roles in hypertrophy; leaves open causal mechanisms and human translation.
Structured PICO
P
Population
Mouse model of cardiac hypertrophy induced by aortic banding, and cultured neonatal hypertrophic cardiomyocytes stimulated by angiotensin II (Ang II) or phenylephrine (PE).
I
Intervention
Aortic banding (in vivo); antisense-mediated depletion (knockdown) of miR-21 (in vitro).
C
Comparator
Sham surgical group (for in vivo model).
O
Outcome
Differential expression of miRNAs and effect of miR-21 knockdown on cardiomyocyte hypertrophy.surrogate
Main Result
p-value: p=<0.01
MicroRNAs, specifically miR-21, are significantly dysregulated in cardiac hypertrophy and their modulation affects cardiomyocyte hypertrophy, suggesting a potential novel therapeutic target.
Cite This Study
Zhang et al. (2007) studied Cardiac hypertrophy. Aortic banding and miR-21 antisense-mediated depletion vs. Sham surgical group was evaluated on Differential expression of miRNAs (p=<0.01). Aortic banding in mice induced aberrant miRNA expression, notably a >4-fold increase in miR-21, and antisense-mediated depletion of miR-21 significantly reduced cardiomyocyte hypertrophy.