Fig. 6.

Proposed model for the involvement of MEF2A/D and HDAC1 in the CAPE-induced up-regulation of SOD3 expression. Under basal conditions, MEF2A/D-HDAC1 complexes bind to the MEF2 regulatory element (MRE) within the SOD3 promoter region, and inhibit the transcription of SOD3 through histone deacetylation. After HRECs have been treated with CAPE, HDAC1 dissociates from the MEF2A/D heterodimer, which increases the enrichment of acetylated histone H3 within the SOD3 promoter region and induces its expression.