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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

Involvement of twist in NNK exposure-promoted lung cancer cell migration and invasion.
In conclusion, Twist was involved in NNK-induced migration and invasion of lung cancer cells. PMID: 31759049 [PubMed - as supplied by publisher]
Source: Toxicology in Vitro - November 19, 2019 Category: Toxicology Authors: Wang Y, Shi L, Li J, Wang H, Yang H Tags: Toxicol In Vitro Source Type: research

Attenuated cholesterol metabolism pathway suppresses regulatory T cell development in prenatal nicotine exposed female mice.
In conclusion, this study showed that PNE could suppress Tregs development in female mice by up-regulating ABCG1-dependent cholesterol efflux, and suggested that PNE-induced thymic Tregs recession of offspring at early life was the developmental origin mechanism of immune dysfunction in later life. PMID: 31629012 [PubMed - as supplied by publisher]
Source: Toxicology - October 15, 2019 Category: Toxicology Authors: Wen X, Zhao WH, Chen LZ, Qu W, Liu HX, Yan HY, Hou LF, Ping J Tags: Toxicology Source Type: research

eIF4E is a critical regulator of human papillomavirus (HPV)-immortalized cervical epithelial (H8) cell growth induced by nicotine.
Abstract Tobacco smoke is known as a cofactor in the development of cervical precancer and cancer caused by human papillomavirus (HPV). The main component in cigarette smoke, nicotine, can be concentrated more strongly in cervical mucus than in blood and it has been implicated as a cocarcinogen that promotes a serial of cancers development through multiple prosurvival pathways. Although the mechanisms of nicotine-induced cell proliferation have been well studied in some epithelial cells, the molecular mechanism of its action in cervical epithelial cells is still unclear. The aims of this study were to investigate ...
Source: Toxicology - March 1, 2019 Category: Toxicology Authors: Chen L, Wang H Tags: Toxicology 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

Alpha5 nicotinic acetylcholine receptor mediates nicotine-induced HIF-1α and VEGF expression in non-small cell lung cancer.
Abstract By binding to nicotinic acetylcholine receptors (nAChRs), nicotine induces the proliferation and apoptosis of non-small cell lung cancer (NSCLC). Previous studies have indicated that α5-nAChR is highly associated with lung cancer risk and nicotine dependence. However, the mechanisms through which α5-nAChRs may influence lung carcinogenesis are far from clear. In the present study, we investigated the roles of α5-nAChR in the nicotine-induced expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF). Immunohistochemistry was used to detect the expression of α5-n...
Source: Toxicology and Applied Pharmacology - April 30, 2014 Category: Toxicology Authors: Ma X, Jia Y, Zu S, Li R, Jia Y, Zhao Y, Xiao D, Dang N, Wang Y Tags: Toxicol Appl Pharmacol Source Type: research

Smad3 mediates cigarette smoke extract (CSE) induction of VEGF release by human fetal lung fibroblasts.
Abstract Cigarette smoke is the major cause of chronic obstructive pulmonary disease (COPD), yet pathogenic mechanisms are not fully understood. Vascular endothelial growth factor (VEGF) is one of the major regulators of endothelial cell survival and is believed to play a role in the pathogenesis of COPD. Fibroblasts are a significant source of VEGF in the lungs; however the effect of cigarette smoke exposure on VEGF release by fibroblasts is not fully understood. We hypothesized that cigarette smoke-induced disturbed VEGF release by human lung fibroblasts is a potential pathogenic mechanism that could contribute ...
Source: Toxicology Letters - April 22, 2013 Category: Toxicology Authors: Farid M, Kanaji N, Nakanishi M, Gunji Y, Michalski J, Iwasawa S, Ikari J, Wang X, Basma H, Nelson AJ, Liu X, Rennard SI Tags: Toxicol Lett Source Type: research