Muscle H3K27ac landscape remodeling with glucocorticoid steroid regimens

Duchenne muscular dystrophy is caused by genetic defects in the gene encoding dystrophin and leads to progressive muscle degeneration. Glucocorticoid steroids are current mainstay pharmacological regimen to decrease muscle inflammation and prolong the ambulatory period in these patients, but daily intake of glucocorticoids like prednisone and deflazacort causes adverse side effects like osteoporosis, adrenal suppression, insulin resistance and obesity. Intermittent steroid dosing has been proposed as alternative to maintain benefits and limit side effects, but a detailed understanding of the mechanisms underpinning the regimen-specific effects in muscle is still missing. Here we explore how once-daily versus once-weekly prednisone (4 week-long treatment) affect the epigenomic landscape in mdx mouse muscle (genetic model of Duchenne muscular dystrophy; DBA/2J background) through H3K27 acetylation profiles. 3 vehicle control samples; 3 once-daily prednisone (1mg/kg i.p.) samples; 3 once-weekly prednisone (1mg/kg i.p.) samples. Each sample is ~10ng immunoprecipitated from the myofiber fraction of quadriceps muscles (2 pooled per mouse) using a rabbit anti-H3K27ac polyclonal antibody (ActiveMotif #39133)