Rho Family Small G Proteins Play Critical Roles in Mechanical Stress–Induced Hypertrophic Responses in Cardiac Myocytes
Key result
Inhibition of Rho family small G proteins suppressed mechanical stretch-induced activation of ERKs, gene expression, and protein synthesis in neonatal rat cardiomyocytes.
Population
neonatal rat cardiomyocytes
Comparison
Inhibition of Rho family small G proteins during… vs Mechanical stretch without Rho inhibition
Design
Preclinical
Authors
Discussion
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Implication
Rho inhibition attenuates stretch-induced hypertrophy in neonatal rat myocytes; leaves open therapeutic targeting in human heart failure.
Structured PICO
P
Population
neonatal rat cardiomyocytes
I
Intervention
Inhibition of Rho family small G proteins (using C3 exoenzyme, Rho-GDI, DNRhoA, or DNRac1) during mechanical stretch
C
Comparator
Mechanical stretch without Rho inhibition
O
Outcome
Hypertrophic responses including ERK activation, gene promoter activity (skeletal alpha-actin and c-fos), and protein synthesis (phenylalanine incorporation)surrogate
The Rho family of small G proteins plays a critical role in mediating mechanical stress-induced hypertrophic signaling and protein synthesis in cardiac myocytes.
Cite This Study
Aikawa et al. (1999) studied Mechanical stress-induced cardiac hypertrophy. C3 exoenzyme, Rho-GDI, DNRhoA, or DNRac1 vs. Control was evaluated on Stretch-induced activation of ERKs, gene expression, and protein synthesis. Inhibition of Rho family small G proteins suppressed mechanical stretch-induced activation of ERKs, gene expression, and protein synthesis in neonatal rat cardiomyocytes.