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. Author manuscript; available in PMC: 2018 Apr 19.
Published in final edited form as: Sci Transl Med. 2018 Feb 7;10(427):eaao0144. doi: 10.1126/scitranslmed.aao0144

Fig. 4. Ex vivo deacetylation of cardiac myofibrils prolongs relaxation kinetics.

Fig. 4

(A) Experimental design. Myofibrils from normal Sprague-Dawley rat LVs were incubated with recombinant HDAC2 or p300 before performing mechanics studies. Myo-fibril relaxation (B) and protein acetylation (C) with and without HDAC2. Myofibril relaxation (D) and protein acetylation (E) with and without p300. (F) Experimental design. Myofibrils isolated from DSS + HS–fed rats were treated with recombinant p300 and acetyl-CoA (coenzyme A). (G) Myofibril relaxation with and without p300. Data are mean + SEM and were compared by Student’s t test. *P < 0.05 versus untreated controls. Data from three separate ARVM preparations were combined; five to nine myofibril bundles were analyzed per ARVM preparation.