Glycogen Synthase Kinase 3β Inhibits Myocardin-Dependent Transcription and Hypertrophy Induction Through Site-Specific Phosphorylation
Population
Neonatal rat cardiomyocytes and HEK 293 cells
Comparison
Adenoviral myocardin overexpression, GSK3beta… vs Wildtype myocardin and basal conditions
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Hypothesis-generating for GSK3β-myocardin control of hypertrophy; leaves open translation to human remodeling or therapy.
Structured PICO
P
Population
Neonatal rat cardiomyocytes and HEK 293 cells
I
Intervention
Adenoviral myocardin overexpression, GSK3beta blockade (10 mmol/L LiCl), myocardin mutants (8xA, 8xD), and cell-permeable peptide containing myocardin GSK3beta motifs
C
Comparator
Wildtype myocardin and basal conditions
O
Outcome
Cardiomyocyte hypertrophy (measured by cell size, total protein amount, and atrial natriuretic factor [ANF] transcription) and myocardin phosphorylationsurrogate
GSK3beta inhibits myocardin-dependent transcription and hypertrophy induction through site-specific phosphorylation, revealing a novel molecular control mechanism for cardiomyocyte hypertrophy.
Cite This Study
Badorff et al. (2005) studied this question.