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Fig. 4 | Journal of Translational Medicine

Fig. 4

From: Hypermethylation of ACADVL is involved in the high-intensity interval training-associated reduction of cardiac fibrosis in heart failure patients

Fig. 4

Primary human cardiac fibroblast responses to high-intensity interval training (HIIT) and knockdown of the acyl-CoA dehydrogenase very long chain (ACADVL) gene (n = 6). A. The red mitochondrial fluorescence, representing the mitochondrial amount, in cells treated with patient serum after (post) HIIT (grey dot) decreased significantly compared to that in cells treated with patient serum before (pre) HIIT (white dot). B. The expression of actin (green) and actin-related protein 2 (Arp2) (red) decreased in cells incubated in post-HIIT serum. Blue fluorescence indicates the nucleus. C. Proteome profiles involved in cell death and movement are presented. Very long-chain acyl-CoA dehydrogenase (VLCAD), cytochrome C (Cyto C), caspase-3 (CASP3) and lamin B1 are involved in apoptosis. Actin B and arp2 are involved in cell movement. D. A decrease in the mitochondrial amount (red) was noted in cells after knockdown of the ACADVL gene. E. Decreased actin (green) and Arp2 (red) fluorescence were identified in cells after knockdown of the ACADVL gene. F. Decreased VLCAD, Lamin B1, Actin B and Arp2, but increased Cyto C as well as CASP3 expression after knockdown of the ACADVL gene

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