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. 2021 Dec 23;10:e60311. doi: 10.7554/eLife.60311

Figure 5. MCAD was required for the conversion of 8 C into acetyl-CoA and subsequent histone acetylation increase and heart protection.

(A) Western blot of H3K9ac level showed MCAD knockdown reduced 8C-induced H3K9ac increase in NRVMs under both normoxia and sI/R. (B) Measurement of medium LDH levels in NRVMs at indicated condition using LDH assay kit. (C) FACS analysis of DHE staining NRVMs after sI/R. (D) Relative mean fluorescence intensity of DHE staining. (E) Enrichment of H3K9ac over H3 at promoters of HO1 and NQO1 after sI/R at indicated conditions. (F) mRNA expression of HO1, NQO1 and MCAD in NRVMs after sI/R. n = 3, *p < 0.05, **p < 0.01, ***p < 0.001, vs Normoxia + PBS + shCTL; #p < 0.05, ##p < 0.01, ###p < 0.001 vs sI/R + PBS + shCTL. Data were analyzed by two-way ANOVA, followed by post-hoc Tukey test.

Figure 5—source data 1. Original numeric data for Figure 5.
Figure 5—source data 2. Original western blot figure for Figure 5.

Figure 5.

Figure 5—figure supplement 1. Knockdown of MCAD is required for alleviating ROS accumulation.

Figure 5—figure supplement 1.

(A) Western blot showed knockdown of MCAD by adenovirus shRNA. (B) Cell viability measurement in NRVMs at shown condition using CCK8 detection kit. (C) NRVM cellular ROS levels are indicated by DHE staining after sI/R treatment. Scale bar: 200 µm. (D–F) Western blot and quantifications of HO1 and NQO1 in NRVMs after sI/R. n = 3, *p < 0.05, **p < 0.01, vs Normoxia + PBS + shCTL; #p < 0.05, ##p < 0.01 vs sI/R + PBS + shCTL. Data were analyzed by two-way ANOVA, followed by post-hoc Tukey test.
Figure 5—figure supplement 1—source data 1. Original western blot figure for Figure 5—figure supplement 1.