Key result
Hydraulic pressure of 170 mm Hg increased cellular area and atrial natriuretic peptide expression in H9c2 cardiomyoblasts, an effect that was reduced by a focal adhesion kinase inhibitor.
Hydraulic pressure induces hypertrophic changes in cardiomyoblasts in vitro, which can be attenuated by focal adhesion kinase inhibition, suggesting a potential therapeutic target for hypertension-induced cardiac hypertrophy.
FAK inhibition may blunt pressure-induced cardiomyoblast changes in vitro; leaves open translation to hypertension-induced hypertrophy in vivo.
We employed a microfluidic device to study the effects of hydraulic pressure on cardiomyoblast H9c2. The 170 mm Hg pressure increased the cellular area and the expression of atrial natriuretic peptide. With the same device, we demonstrated that the effects of hydraulic pressure on the cardiomyoblast could be reduced by the inhibitor of focal adhesion kinase. This mechanical-chemical antagonism could lead to a potential therapeutic strategy of hypertension-induced cardiac hypertrophy.
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Hsiao et al. (2015) studied this question. Hydraulic pressure was evaluated on Cellular area and expression of atrial natriuretic peptide. Hydraulic pressure of 170 mm Hg increased cellular area and atrial natriuretic peptide expression in H9c2 cardiomyoblasts, an effect that was reduced by a focal adhesion kinase inhibitor.
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