[Histone deacetylase 11 promotes ox-LDL-induced mouse macrophage foam cell formation via inhibiting autophagy]

Objective To investigate the effect of histone deacetylase 11 (HDAC11) on oxidized low density lipoprotein (ox-LDL)-induced mouse macrophage foam cell formation. Methods Macrophages derived from the RAW264.7 cell line were divided into three groups: Control group, ox-LDL group, and ox-LDL combined with Rapamycin group. Oil red O staining was used to observe the formation of foam cells, the content of total cholesterol (TC) and triglyceride (TG) in macrophages were measured using microplate reader. The expression of HDAC11, microtubule-associated protein 1 light chain 3-β (LC3B) II and p62 were detected by Western blot assay. Si-HDAC11 was transfected into macrophages, and qRT-PCR and Western blot assay were employed to measure the interference efficiency of HDAC11. On the basis of ox-LDL treatment, the expression of HDAC11 in RAW264.7 cells was knock down. Oil red O staining was used to observe the lipid droplet content, the content of TC and TG were detected by using microplate reader, and LC3BII and p62 protein expressions were detected by Western blot assay. Results Compared to the control group, the protein expression of LC3BII was reduced, while p62 and HDAC11 protein were increased, which is accompanied by a significant increase of the lipid droplet content, TC and TG. Simultaneously, treated RAW264.7 cells with Rapamycin, an autophagy agonist, LC3BII and p62 protein expressions, as well as lipid droplets, TC, and TG content changes were significantly alleviated in RAW264.7 cells. LC3BII expression was significantly increased after the transfection of si-HDAC11 into macrophages, while p62 protein expression was decreased, and intracellular lipid droplets, TC and TG contents were also reduced correspondingly. Conclusion HDAC11 promotes ox-LDL-induced mouse macrophage foam cell formation via inhibiting autophagy.