Figure 7: MS-275 reduced acetylation of histone H3 and H4 in cigarette smoke-exposed mouse lungs. | Scientific Reports

Figure 7: MS-275 reduced acetylation of histone H3 and H4 in cigarette smoke-exposed mouse lungs.

From: HDAC1-3 inhibitor MS-275 enhances IL10 expression in RAW264.7 macrophages and reduces cigarette smoke-induced airway inflammation in mice

Figure 7

To study the effect of MS-275 on total HDAC activity in nuclear lung extracts of cigarette smoke-exposed mice, HDAC activity was determined based on the conversion of a pro-fluorogenic substrate (A). MS-275 restored HDAC activity compared to air-exposed mice. Data are presented as mean ± SD of 4–5 animals per group. Effects of MS-275 on histone H3 and H4 acetylation were studied by Western blot (blots were cropped; full length blots are shown in Figure S11 (B) and quantified by densitometry (C). Total histone H3 and H4 acetylation was increased in cigarette smoke-exposed mice lungs, and for histone H4 this was reduced by MS-275. #p < 0.05 compared air-exposed animals **p < 0.01 compared to vehicle (smoke and inhibitor-solvent treated) animals. Histone acetylation of histone H3 and H4 was also analyzed by mass spectrometry (D). Histones were resolved by SDS-PAGE, histones H3 and H4 were excised from the gel and subjected to LC-MS/MS analysis. Smoke exposure increased, and MS-275 reduced, acetylation on one peptide from histone H4 (res. 4–17: GKGGKGLGKGGAKR). Other peptides were not affected. Data are presented as mean ± SD of 4–5 animals per group. *p < 0.05 compared to air-exposed animals. #p < 0.05 compared to vehicle (smoke and inhibitor-solvent treated) animals.

Back to article page