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Drug: Nicotine

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Total 48 results found since Jan 2013.

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

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

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

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

SOCS3 participates in cholinergic pathway regulation of synovitis in rheumatoid arthritis.
This study investigated the effect of SOCS on cholinergic pathway regulation of synovitis in the fibroblast-like synoviocytes (FLSs) of RA and CIA mice. The effects of nicotine on SOCS1 and SOCS3 protein expression in FLSs were assayed by western blotting before and after transfection with a small interfering RNA oligonucleotide (SOCS3-siRNA or control-siRNA). Interleukin-6 was measured by enzyme-linked immunosorbent assay of SOCS3-siRNA and control-siRNA transfected FLS culture supernatants. Histopathological evaluation and immunohistochemical staining of SOCS3 were performed in joint tissue sections of control, CIA model...
Source: Connective Tissue Research - September 17, 2017 Category: Research Tags: Connect Tissue Res Source Type: research

Carbon monoxide-releasing molecule suppresses inflammatory and osteoclastogenic cytokines in nicotine- and lipopolysaccharide-stimulated human periodontal ligament cells via the heme oxygenase-1 pathway.
Abstract Smoking is identified as a risk factor for periodontitis. Carbon monoxide (CO)-releasing molecule-3 (CORM-3) is a compound that has demonstrated anti-inflammatory effects in vitro and in vivo studies. The present study aimed to investigate the effects of CORM-3 on the expression of inflammatory and osteoclastogenic cytokines in human periodontal ligament cells (PDLCs) stimulated by nicotine and lipopolysaccharide (LPS). The cells were pretreated with CORM-3 and then cultured in medium in the presence of nicotine and LPS. The mRNA and protein expression levels of prostaglandin E2 (PGE2), cyclooxygenas...
Source: International Journal of Molecular Medicine - September 8, 2017 Category: Molecular Biology Authors: Song L, Li J, Yuan X, Liu W, Chen Z, Guo D, Yang F, Guo Q, Song H Tags: Int J Mol Med Source Type: research

Wnt/ β-catenin signaling plays an essential role in α7 nicotinic receptor-mediated neuroprotection of dopaminergic neurons in a mouse Parkinson's disease model.
The objective of the present study was to explore the potential functions of α7-nAChRs in PD pathology, and to determine whether these effects are exerted via Wnt/β-catenin signaling in a mouse PD model. In the in vivo study, α7-nAChR knockout (α7-KO) reversed the beneficial effects of nicotine on motor deficits, dopaminergic neuron loss, astrocyte and microglia activation, and reduced striatal dopamine release induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Injury to SH-SY5Y cells by 1-methyl-4-phenylpyridinium treatment was also ameliorated by nicotine, and this effect was abolished by methyllycaconitine (ML...
Source: Biochemical Pharmacology - May 24, 2017 Category: Drugs & Pharmacology Authors: Liu Y, Hao S, Yang B, Fan Y, Qin X, Chen Y, Hu J Tags: Biochem Pharmacol Source Type: research

Pravastatin activates activator protein 2 alpha to argument the angiotensin II-induced abdominal aortic aneurysms.
In conclusion, pravastatin promotes AAA formation through AMPKα2-dependent AP-2α activations. PMID: 28179583 [PubMed - as supplied by publisher]
Source: Oncotarget - February 11, 2017 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Extracellular Release of Annexin A2 is Enhanced upon Oxidative Stress Response via the p38 MAPK Pathway after Low-Dose X-Ray Irradiation.
In this study, we found that in cultured human cancer and non-cancerous cells an extracellular release of annexin A2 was greatly enhanced 1-4 h after a single 20 cGy X-ray dose, but not after exposure to ultraviolet C (UVC) radiation. Extracellular release of annexin A2 was also enhanced after H2O2 and nicotine treatments, which was suppressed by pretreatment with the antioxidant, N-acetyl cysteine. Among the oxidative stress pathway molecules examined in HeLa cells, AMP-activated protein kinase α (AMPKα) and p38 mitogen-activated protein kinase (MAPK) were mostly activated by low-dose X-ray radiation, and the p38 MAPK i...
Source: Radiation Research - June 28, 2016 Category: Physics Authors: Kita K, Sugita K, Sato C, Sugaya S, Sato T, Kaneda A Tags: Radiat Res Source Type: research

Silencing A7-nAChR levels increases the sensitivity of gastric cancer cells to ixabepilone treatment
Abstract Gastric cancer is an important health issue worldwide. Currently, improving the therapeutic efficacy of chemotherapy drugs is an important goal of cancer research. Alpha-7 nicotine acetylcholine receptor (A7-nAChR) is the key molecule that mediates gastric cancer progression, metastasis, and therapy responses; however, the role of A7-nAChR in the therapeutic efficacy of ixabepilone remains unclear. A7-nAChR expression was silenced by small interfering RNA (siRNA) technology. The cytotoxicity of ixabepilone was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and ixabe...
Source: Tumor Biology - January 20, 2016 Category: Cancer & Oncology Source Type: research

Abstract P162: Nicotine via Cd36, Cox2 and Oxidative Stress Promotes Podocyte Injury: Link Between E-cigarettes and Renal Disease Progression? Session Title: Chronic Kidney and Renal
Conclusion: NIC activated in human POD a reciprocal interplay between NADPH oxidases and COX2 that increased O2- production, reduced Synpo and upregulated the B scavenger receptor CD36 that, via increased uptake of oxidized LDL, promoted podocyte apoptosis. We surmise that these novel findings implicate NIC as a risk factor for CVD and CKD progression.
Source: Hypertension - November 3, 2015 Category: Cardiology Authors: Raij, L., Tian, R., Zhou, M.-S. Tags: Session Title: Chronic Kidney and Renal Source Type: research

Nicotine reduces the levels of surfactant proteins A and D via Wnt/β-catenin and PKC signaling in human airway epithelial cells
Publication date: 15 January 2016 Source:Respiratory Physiology & Neurobiology, Volume 221 Author(s): Weifeng Zou, Sha Liu, Jinxing Hu, Qing Sheng, Fang He, Bing Li, Pixin Ran A deficiency of surfactant proteins A and D has been proposed as a mechanism in airway remodeling, which is one characteristic of chronic obstructive pulmonary disease (COPD). We recently showed that in vitro nicotine exposure induces Wnt3a/β-catenin activation, which is a pathway that has also been implicated in altering levels of SP-A and SP-D. Nicotine induced activation of protein kinase C(PKC), and the involvement of PKC in med...
Source: Respiratory Physiology and Neurobiology - October 30, 2015 Category: Respiratory Medicine Source Type: research

Abstract 924: GM-CSF induces CREB signaling pathways and modulates tobacco carcinogen-induced pancreatic tumorigenesis
Introduction: Nicotine and nitrosamine exposure from smoking causes pancreatic cell injury and contributes to a cascade of oncogenic events that may be contributing to the rising rate of pancreatic cancer (PDAC). Cytokines activate kinases and transcription factors including cyclic AMP response element binding (CREB) protein. CREB activation through phosphorylation regulates diverse cellular responses. We studied whether granulocyte-macrophage colony stimulating factor (GM-CSF)-dependent phosphorylated CREB plays a role in smoking-induced pathogenesis of PDAC.Experimental procedure: Human tissue microarray analysis was per...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Castellanos, J., Honnenahally, K., Shi, C., Merchant, N., Nagathihalli, N. Tags: Carcinogenesis Source Type: research

α5-nAChR modulates nicotine-induced cell migration and invasion in A549 lung cancer cells.
Abstract Cigarette smoking is the most important risk factor in the development of human lung cancer. Nicotine, the major component in tobacco, not only contributes to carcinogenesis but also promotes tumor metastasis. By binding to nicotinic acetylcholine receptors (nAChRs), nicotine induces the proliferation and migration of non-small cell lung cancer. Recently studies have indicated that α5-nAChR is highly associated with lung cancer risk and nicotine dependence. Nevertheless, it is unclear whether nicotine promotes the migration and invasion through activation of α5-nAChR in lung cancer. In the present study...
Source: Experimental and Toxicologic Pathology - July 20, 2015 Category: Pathology Authors: Sun H, Ma X Tags: Exp Toxicol Pathol Source Type: research