HDAC inhibition promotes cardiogenesis and the survival of embryonic stem cells through proteasome-dependent pathway.

ABSTRACT: Histone deacetylase (HDAC) inhibition plays a crucial role in mediating cardiogenesis and myocardial protection, whereas HDAC degradation has recently attracted attention in mediating the biological function of HDACs. However, it remains unknown whether HDAC inhibition modulates cardiogenesis and embryonic stem cell (ESC) survival through the proteasome pathway. Using the well-established mouse ESC culture, we demonstrated that HDAC inhibitors, both trichostatin A (TSA,50  nmol/L) and sodium butyrate (NaB, 200  µmol/L) that causes the pronounced reduction of HDAC4 activity, decreased cell death and increased viability of ESCs in response to oxidant stress. HDAC inhibition reduced the cleaved caspases 3, 6, 9, PARP, and TUNEL positive ESCs, which were abrogated with MG132 (0.5  µmol/L), a s

SUBMITTER: Chen HP 

PROVIDER: S-EPMC3357124 | biostudies-literature | 2011 Nov

REPOSITORIES: biostudies-literature