Concurrent opposite effects of trichostatin A, an inhibitor of histone deacetylases, on expression of α-MHC and cardiac tubulins: implication for gain in cardiac muscle contractility

Abstract

. Concurrent opposite effects of trichostatin A, an inhibitor of histone deacetylases, on expression of ␣-MHC and cardiac tubulins: implication for gain in cardiac muscle contractility.

Prion-like Nanofibrils of Small Molecules (PriSM) Selectively Inhibit Cancer Cells by Impeding Cytoskeleton Dynamics

“…4g). In vivo tubulin/ microtubule assays (38) reveal that cells incubated with PriSM of 1 exhibit a similar ratio of free tubulins to microtubules with that of the untreated cells (Fig. 4h), further suggesting that the dots of fluorescence are from clusters of short microtubules.…”

Toward transcriptional therapies for the failing heart: chemical screens to modulate genes

“…Importantly, HDAC inhibition in vitro and in vivo results in downregulation β-MHC expression, with a concomitant increase in the levels of α-MHC (68,72). Thus, we predict that HDAC inhibitors will not only antagonize deleterious cardiac growth, but will also increase myofibrillar ATPase activity and improve contractility in the failing heart.…”

Factors controlling cardiac myosin-isoform shift during hypertrophy and heart failure

“…Inhibition of HDACs by a non-specific inhibitor, trichostatinA (TSA), an agent that inhibits both class-I and -II HDACs, has been shown to block cardiac hypertrophy and activate αMHC expression, without altering the levels of βMHC, in both in vitro and in vivo models of cardiac hypertrophy [129,130]. This effect of TSA is likely to be contributed by its ability to inhibit class-I HDACs, as specific inhibitors of class-I HDACs were found to block cardiac hypertrophy, whereas inhibition of class-II HDACs was shown to sensitize the heart to hypertrophic stimuli [130,131].…”