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Snail/HDAC1/2 mediate skeletal growth retardation in fetuses caused by prenatal nicotine exposure
This study intends to clarify the specific molecular mechanism of fetal osteochondral retardation caused by PNE through animal and cellular experiments. The present study demonstrated that in male offspring of the PNE group (the pregnant rats were subcutaneously administered nicotine 1.0 mg/kg twice per day (2.0 mg/kg.d) at GD11-20), the cartilage matrix of the fetal growth plate was lightly stained, the collagen was reduced, and expression of the matrix phenotype genes, ACAN and Col2A1, was significantly decreased. It was further found that PNE decreased histone acetylation (H3K9/H3K14) levels in the ACAN and Col2A1 promo...
Source: Toxicology - July 10, 2021 Category: Toxicology Authors: Yu Deng Hui Gao Hui Wang Liaobin Chen Source Type: research

nAChRs-ERK1/2-Egr-1 signaling participates in the developmental toxicity of nicotine by epigenetically down-regulating placental 11 β-HSD2.
This study aimed to elucidate the epigenetically regulatory mechanism of nicotine on placental 11β-HSD2 expression. Pregnant Wistar rats were administered 1.0 mg/kg nicotine subcutaneously twice a day from gestational day 9 to 20. The results showed that prenatal nicotine exposure increased corticosterone levels in the placenta and fetal serum, disrupted placental morphology and endocrine function, and reduced fetal bodyweight. Meanwhile, histone modification abnormalities (decreased acetylation and increased di-methylation of histone 3 Lysine 9) on the HSD11B2 promoter and lower-expression of 11β-HSD2 were observed. F...
Source: Toxicology and Applied Pharmacology - February 24, 2018 Category: Toxicology Authors: Zhou J, Liu F, Yu L, Xu D, Li B, Zhang G, Huang W, Li L, Zhang Y, Zhang W, Wang H Tags: Toxicol Appl Pharmacol Source Type: research