BACKGROUND: Previously, we have observed that the isolated, erythrocyte-perfused @entity95 heart has increased levels of @entity1457 protein (HSP) 72 after a mild mechanical stress. We hypothesized that stretch-activated ion channels (SACs) mediated this increase. Methods and Results-- To test this hypothesis, we subjected isolated, perfused @entity35 hearts to mechanical stretch. Gel mobility shift assay showed that @entity1457 factor (HSF) was activated in hearts with mechanical stretch, but not in controls. Supershift experiments demonstrated that @entity35598 was the transcription factor. Northern blots revealed the concomitant increase in @entity34445 mRNA in stretched @entity35 hearts. In a separate set of experiments, @entity2287 , an inhibitor of SACs, was added to the perfusate. @entity2287 inhibited the activation of HSF and decreased @entity34445 mRNA level. Because @entity2287 can inhibit both SACs and L-type @entity460 channels, we perfused a group of hearts with @entity3988 , a specific L-type @entity460 channel blocker, to eliminate the involvement of L-type @entity460 channels. Diltiazem failed to inhibit the activation of HSF. CONCLUSIONS: Stretch in the @entity35 heart results in activation of @entity35598 and an increase in @entity34445 mRNA through SACs. This represents a novel mechanism of HSF activation and may be an important cardiac signaling pathway for hemodynamic stress.

Activation of @entity1457 factor by stretch-activated channels in XXXX hearts.

@entity35598 :: ('79245(Tax:10116)', 'Gene') :: ['HSF1'] @entity34445 :: ('24472(Tax:10116)', 'Gene') :: ['HSP72'] @entity1457 :: ('MESH:D012769', 'Disease') :: ['heat-shock'] @entity95 :: ('9986', 'Species') :: ['rabbit'] @entity3988 :: ('MESH:D004110', 'Chemical') :: ['diltiazem'] @entity460 :: ('MESH:D002118', 'Chemical') :: ['calcium'] @entity35 :: ('10116', 'Species') :: ['rat'] @entity2287 :: ('MESH:D005682', 'Chemical') :: ['Gadolinium', 'gadolinium']
@entity35 :: (10116,Species) :: ['rat']
