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Drug: Nicotine

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Total 48 results found since Jan 2013.

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

Nicotine Enhances Mesangial Cell Proliferation and Fibronectin Production in High Glucose Milieu via Activation of Wnt/ β-catenin Pathway.
In this study, we examined the involvement of Wnt/β-catenin pathway in nicotine-mediated mesangial cell growth in high glucose milieu. Primary human renal mesangial cells were treated with nicotine in the presence of normal (5 mM) or high glucose (30 mM) followed by evaluation for cell growth. In the presence of normal glucose, nicotine increased both the total cell numbers and Ki-67 positive cell ratio, indicating that nicotine stimulated mesangial cell proliferation. Although high glucose itself also stimulated mesangial cell proliferation, nicotine further enhanced the mitogenic effect of high glucose. Similarly, nicot...
Source: Bioscience Reports - March 23, 2018 Category: Biomedical Science Authors: Lan X, Wen H, Aslam R, Marashi Shoshtari SS, Mishra A, Kumar V, Wang H, Wu G, Luo H, Malhotra A, Singhal PC Tags: Biosci Rep Source Type: research

Epigenetic activation of PERP transcription by MKL1 contributes to ROS-induced apoptosis in skeletal muscle cells
In conclusion, our data illustrate a novel epigenetic pathway that links PERP transcription to ROS-induced apoptosis in skeletal muscle cells.
Source: Biochimica et Biophysica Acta (BBA) Gene Regulatory Mechanisms - July 27, 2018 Category: Genetics & Stem Cells Source Type: research

Epigenetic activation of PERP transcription by MKL1 contributes to ROS-induced apoptosis in skeletal muscle cells.
In conclusion, our data illustrate a novel epigenetic pathway that links PERP transcription to ROS-induced apoptosis in skeletal muscle cells. PMID: 30056131 [PubMed - as supplied by publisher]
Source: Biochimica et Biophysica Acta - July 26, 2018 Category: Biochemistry Authors: Li Z, Chen B, Dong W, Xu W, Song M, Fang M, Guo J, Xu Y Tags: Biochim Biophys Acta Source Type: research

TRPC channels mediated calcium entry is required for proliferation of human airway smooth muscle cells induced by nicotine-nAChR.
In conclusion, nicotine-induced HASMC proliferation was mediated by TRPC3-dependent calcium entry via α5-nAchR, which provided a potential target for treatment of COPD. PMID: 30550855 [PubMed - as supplied by publisher]
Source: Biochimie - December 11, 2018 Category: Biochemistry Authors: Jiang Y, Zhou Y, Peng G, Tian H, Pan D, Liu L, Yang X, Li C, Li W, Chen L, Ran P, Dai A Tags: Biochimie 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

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

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

nAChR signaling regulates IRE1 α activation to protect β cells against terminal unfolded protein response under irremediable ER stress
ConclusionsOur findings suggest that nAChR signaling regulates IRE1 α activation to protect β cells from the T‐UPR and apoptosis under ER stress partly through α7 nAChR. Targeting nAChR signaling to inhibit the T‐UPR cascade may therefore hold therapeutic promise by thwarting β cell death in diabetes.
Source: Journal of Diabetes Investigation - January 9, 2020 Category: Endocrinology Authors: Tatsuya Ishibashi, Shuhei Morita, Shohei Kishimoto, Shinsuke Uraki, Ken Takeshima, Yasushi Furukawa, Hidefumi Inaba, Hiroyuki Ariyasu, Hiroshi Iwakura, Hiroto Furuta, Masahiro Nishi, Feroz R. Papa, Takashi Akamizu Tags: ORIGINAL ARTICLE Source Type: research

Human secreted protein SLURP-1 abolishes nicotine-induced proliferation, PTEN down-regulation and α7-nAChR expression up-regulation in lung cancer cells.
Abstract Human Ly-6/uPAR-related protein-1 (SLURP-1) is an allosteric negative modulator of the α7-type nicotinic acetylcholine receptor (α7-nAChR), one of the key receptors promoting nicotine-induced proliferation of lung cancer cells. Incubation of lung adenocarcinoma A549 cells with recombinant SLURP-1 (rSLURP-1) at concentrations >10 nM resulted in the significant decrease of the cell growth (~70%), while treatment of normal lung-derived WI-38 fibroblasts with rSLURP-1 did not influence the cell proliferation up to 1 μM of the protein. rSLURP-1 fully abolished the nicotine-induced increase of the cell ...
Source: International Immunopharmacology - February 23, 2020 Category: Allergy & Immunology Authors: Shulepko MA, Bychkov ML, Shlepova OV, Shenkarev ZO, Kirpichnikov MP, Lyukmanova EN Tags: Int Immunopharmacol Source Type: research

Nicotine-induced adrenal beta-arrestin1 upregulation mediates tobacco-related hyperaldosteronism leading to cardiac dysfunction.
CONCLUSION: Adrenal βarrestin1 upregulation is one of the mechanisms by which tobacco compounds, like nicotine, promote cardio-toxic hyperaldosteronism in vitro and in vivo. Thus, adrenal βarrestin1 represents a novel therapeutic target for tobacco-related heart disease prevention or mitigation. PMID: 32547713 [PubMed]
Source: World Journal of Cardiology - May 25, 2020 Category: Cardiology Authors: Cora N, Ghandour J, Pollard CM, Desimine VL, Ferraino KE, Pereyra JM, Valiente R, Lymperopoulos A Tags: World J Cardiol Source Type: research

Nicotine Upregulates the Level of Mcl-1 through STAT3 in H1299 Cells
Conclusions: We have demonstrated that nicotine induces up-regulation of Mcl-1 through STAT3, which process may be independent on JAKs and not only dependent on the phosphorylation of Y705. Downregulation of Mcl-1 transcription by inhibiting STAT3 cascade may be a potential strategy for the treatment of this cancer.
Source: Journal of Cancer - July 2, 2020 Category: Cancer & Oncology Authors: Maojun Zhou, Jinfeng Zhao, Qi Zhang, Xin Jin, Mingmei Liao, Lihua Zhang, Jiwei Wang, Manyi Yang Tags: Research Paper Source Type: research

Nicotine inhibits MAPK signaling and spheroid invasion in ovarian cancer cells.
Abstract Nicotine is the major addictive component of cigarette smoke and although it is not considered carcinogenic, it can enhance or inhibit cancer cell proliferation depending on the type of cancer. Nicotine mediates its effects through nicotinic acetylcholine receptors (nAChRs), which are expressed in many different neuronal and non-neuronal cell types. We observed that the α4, α5, α7 subunits nAChRs were expressed in ovarian cancer (OC) cells. Nicotine inhibited the proliferation of SKOV3 and TOV112D OC cells, which have TP53 mutation and wild-type KRAS, but did not inhibit the proliferation of TOV21G or ...
Source: Experimental Cell Research - July 6, 2020 Category: Cytology Authors: Harmych SJ, Kumar J, Bouni ME, Chadee DN Tags: Exp Cell Res Source Type: research

Changes in mucin production in human airway epithelial cells after exposure to e-cigarette vapor with or without nicotine.
Conclusion: E-cigarettes vapor with and with nicotine is significantly increased MUC5AC expression in human airway epithelial cells. PMID: 33355840 [PubMed - as supplied by publisher]
Source: Clinical and Experimental Otorhinolaryngology - December 29, 2020 Category: ENT & OMF Tags: Clin Exp Otorhinolaryngol Source Type: research

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