Serine 105 phosphorylation of transcription factor GATA4 is necessary for stress-induced cardiac hypertrophy in vivo
Key result
Gata4-S105A mutant mice exhibited a blunted hypertrophic response to phenylephrine and pressure overload, but were more susceptible to heart failure and cardiac dilation.
Population
Homozygous Gata4-S105A knock-in mutant mice
Design
Preclinical
Follow-up
2 weeks
Authors
Discussion
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Implication
GATA4 S105 phosphorylation may enable adaptive hypertrophy under stress; leaves open its potential as a target to prevent heart failure in patients.
Structured PICO
P
Population
Homozygous Gata4-S105A knock-in mutant mice
I
Intervention
Phenylephrine agonist infusion for 2 weeks or pressure overload for 1 and 2 weeks; direct ERK1/2 activation using an activated MEK1 transgene
O
Outcome
Cardiac hypertrophy in response to stress stimulationsurrogate
Phosphorylation of GATA4 at serine 105 is necessary for the adaptive hypertrophic response to cardiac stress, and its absence increases susceptibility to heart failure.
Cite This Study
Berlo et al. (2011) studied Cardiac hypertrophy. Gata4-S105A mutation was evaluated on Cardiac hypertrophy in response to stress stimulation. Gata4-S105A mutant mice exhibited a blunted hypertrophic response to phenylephrine and pressure overload, but were more susceptible to heart failure and cardiac dilation.