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Fig. 5 | Stem Cell Research & Therapy

Fig. 5

From: Histone hypo-acetylation of Sox9 mediates nicotine-induced weak cartilage repair by suppressing BMSC chondrogenic differentiation

Fig. 5

Effects of nicotine on histone acetylation on the promoter of Sox9 in BMSCs. Assay were performed after 24 h of in vitro culture. a Change of H3K9 acetylation on the promoter of Sox9. b Change of H3K14 acetylation on the promoter of Sox9. c Change of NFATc2 binding on the promoter of Sox9. d Change of 1 binding on the promoter of Sox9. e Change of Sox9 binding on the enhancer of Col2A1. f Effects of methyllycaconitine (MLA) and Si-NFATc2 on nicotine’s suppression of H3K9 acetylation on the promoter of Sox9. g Effects of MLA and Si-NFATc2 on nicotine’s suppression of H3K14 acetylation on the promoter of Sox9. h Effects of MLA and Si-NFATc2 on nicotine’s suppression of Sox9 binding on the enhancer of Col2A1. Data represent mean ± SEM (n = 3). *p < 0.05, **p < 0.01. BMSCs bone marrow mesenchymal stem cells, Col2A1 α1 chain of type II collagen, HDAC1 histone deacetylase1, MLA methyllycaconitine, NFATc2 nuclear factor of activated T cell 2, Sox9 SRY-type high-mobility group box 9

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