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

Pub. Date : 2018 Apr 10

PMID : 29631619






3 Functional Relationships(s)
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1 Nicotine"s effect on chondrogenic differentiation was studied by exposing BMSCs to nicotine at 0.1, 1, 10, and 100 muM, and methyllycaconitine (MLA), which is a selective alpha7-nicotinic acetylcholine receptor (nAChR) inhibitor and si-RNA of nuclear factor of activated T cells 2 (NFATc2), were used to verify the molecular mechanism of nicotine"s effect. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus
2 Nicotine"s effect on chondrogenic differentiation was studied by exposing BMSCs to nicotine at 0.1, 1, 10, and 100 muM, and methyllycaconitine (MLA), which is a selective alpha7-nicotinic acetylcholine receptor (nAChR) inhibitor and si-RNA of nuclear factor of activated T cells 2 (NFATc2), were used to verify the molecular mechanism of nicotine"s effect. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus
3 Further in vitro study demonstrated that nicotine enhanced intracellular Ca2+ and activity of calcineurin (CaN) through alpha7-nAChR, increased the nucleic expressions of NFATc2 and the bindings to SOX9 promoter, and thus reduced the acetylation of H3K9 and H3K14 in SOX9 promoter. Nicotine cholinergic receptor nicotinic beta 1 subunit Rattus norvegicus