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Drug: Nicotine

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Total 48 results found since Jan 2013.

Activation of Nicotinic Receptors Inhibits TNF-α-Induced Production of Pro-inflammatory Mediators Through the JAK2/STAT3 Signaling Pathway in Fibroblast-Like Synoviocytes
In conclusion, nicotine has an anti-inflammatory effect on RA by downregulating production of IL-6 and MCP-1 in FLSs, and this is mediated through activation of the JAK2–STAT3 signal pathway.
Source: Inflammation - January 23, 2015 Category: Allergy & Immunology Source Type: research

HIF‐2 inhibition supresses inflammatory responses and osteoclastic differentiation in human periodontal ligament cells
This article is protected by copyright. All rights reserved
Source: Journal of Cellular Biochemistry - January 7, 2015 Category: Biochemistry Authors: Won‐Jung Bae, Mee‐Ran Shin, Soo‐Kyung Kang, Zhang Jun, Jun‐Yeol Kim, Sang‐Cheon Lee, Eun‐Cheol Kim Tags: Article Source Type: research

Regulation of Cigarette Smoke Induction of IL‐8 in Macrophages by AMP‐activated Protein Kinase Signaling
This article is protected by copyright. All rights reserved
Source: Journal of Cellular Physiology - December 11, 2014 Category: Cytology Authors: Hsin‐Kuo Ko, Hung‐Fu Lee, An‐Hsuan Lin, Meng‐Han Liu, Ching‐I Liu, Tzong‐Shyuan Lee, Yu Ru Kou Tags: Original Research Article Source Type: research

Role of resistin in the inflammatory response induced by nicotine plus lipopolysaccharide in human periodontal ligament cells in vitro
ConclusionThis is the first study to show that the inhibition of resistin, by either a pharmacological or a genetic silencing approach, has anti‐inflammatory effects. These effects include decreased levels of inflammatory cytokines and the prevention of ECM breakdown in a nicotine plus LPS‐stimulated PDLC model.
Source: Journal of Periodontal Research - November 13, 2014 Category: Dentistry Authors: S.‐K. Kang, Y.‐D. Park, S.‐I. Kang, D.‐K. Kim, K.‐L. Kang, S.‐Y. Lee, H.‐J. Lee, E.‐C. Kim Tags: Original Article Source Type: research

Abstract 4456: Aurora-A is a downstream target of RAS and forms a positive feedback regulation loop with NF-{kappa}B in non-small cell lung cancer
Previous studies have shown that inhibition of Aurora-A reduces mutant RAS oncogenic activity and that both Aurora-A and RAS activate NF-κB pathway through phosphorylation of IkBa and upregulation of GSKa, respectively. Here we show that Aurora-A expression and kinase activity are regulated by activating mutation of KRAS. Blockage of NF-κB by IκB-S32/36A abrogated KRAS-induced Aurora-A expression and kinase activity. Furthermore, we demonstrated that NF-κB directly bound to Aurora-A promoter and induces Aurora-A transcription. In addition, depletion of Aurora-A by siRNA and pharmacological inhibitor MLN8237 suppresses ...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Kim, D., Kanai, M., Zheng, X., Zheng, D., Coppola, D., Cheng, J. Q. Tags: Molecular and Cellular Biology Source Type: research

Nicotine-mediated invasion and migration of non-small cell lung carcinoma cells by modulating STMN3 and GSPT1 genes in an ID1-dependent manner
Conclusions: Collectively, our data suggests that nicotine and EGF induce genes such as STMN3 and GSPT1 to promote the proliferation, invasion and migration of NSCLC, thus enhancing their tumorigenic properties. These studies thus reveal a central role for ID1 and its downstream targets in facilitating lung cancer progression.
Source: Molecular Cancer - July 16, 2014 Category: Cancer & Oncology Authors: Sajitha NairNamrata Bora-SinghalDeepak PerumalSrikumar Chellappan 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

Effects of chronic exposure to cigarette smoke on canonical transient receptor potential expression in rat pulmonary arterial smooth muscle
In this study, we demonstrated that chronic CS exposure led to rat weight loss, right ventricular hypertrophy, and pulmonary arterial remodeling. A fluorescence microscope was used to measure intracellular calcium concentration ([Ca2+]i) in rat distal PASMCs. Results showed that basal [Ca2+]i and store-operated calcium entry (SOCE) levels in PASMCs from 3- and 6-mo CS-exposed rats were markedly higher than those in cells from the unexposed control animals (the increases in 6-mo CS group were more significant than that in 3-mo group), accompanied with increased canonical transient receptor potential 1 (TRPC1) and TRPC6 expr...
Source: AJP: Cell Physiology - February 15, 2014 Category: Cytology Authors: Wang, J., Chen, Y., Lin, C., Jia, J., Tian, L., Yang, K., Zhao, L., Lai, N., Jiang, Q., Sun, Y., Zhong, N., Ran, P., Lu, W. Tags: ARTICLES Source Type: research

GW1929 inhibits α7 nAChR expression through PPARγ-independent activation of p38 MAPK and inactivation of PI3-K/mTOR: The role of Egr-1.
Abstract Studies demonstrated that peroxisome proliferator-activated receptor gamma (PPARγ) ligands reduce nicotine-induced non small cell lung carcinoma (NSCLC) cell growth through inhibition of nicotinic acetylcholine receptor (nAChR) mediated signaling pathways. However, the mechanisms by which PPARγ ligands inhibited nAChR expression remain elucidated. Here, we show that GW1929, a synthetic PPARγ ligand, not only inhibited but also antagonized the stimulatory effect of acetylcholine on NSCLC cell proliferation. Interestingly, GW1929 inhibited α7 nAChR expression, which was not blocked by GW9662, an antagon...
Source: Cellular Signalling - January 8, 2014 Category: Cytology Authors: Hahn SS, Tang Q, Zheng F, Zhao S, Wu J Tags: Cell Signal Source Type: research

Effect of Chronic Exposure to Cigarette Smoke on Canonical Transient Receptor Potential Expression in Rat Pulmonary Arterial Smooth Muscle.
In this study, we demonstrated that chronic cigarette smoke (CS) exposure leads to rat weight loss, right ventricular hypertrophy, and pulmonary artery remodeling. A fluorescence microscope was used to measure intracellular calcium concentration ([Ca(2+)]i) in rat distal PASMCs. Results showed that basal [Ca(2+)]i and store-operated calcium entry (SOCE) level in PASMCs from 3 and 6 months CS exposed rats were higher than those in the unexposed control group, among which the increase in 6 months CS group was more significant than that in 3 months group. Furthermore, chronic exposure to CS also increased TRPC1 and TRPC6 expr...
Source: American Journal of Physiology. Cell Physiology - December 11, 2013 Category: Cytology Authors: Wang J, Chen Y, Lin C, Jia J, Tian L, Yang K, Zhao L, Lai N, Jiang Q, Sun Y, Zhong NS, Ran P, Lu W Tags: Am J Physiol Cell Physiol Source Type: research

A functional link between heme oxygenase-1 and tristetraprolin in the anti-inflammatory effects of nicotine.
In this study, we sought to determine whether HO-1 associates with TTP to mediate the anti-inflammatory effects of nicotine. Inhibition of HO-1 activity or HO-1 expression attenuated the effects of nicotine on STAT3 activation, TTP induction, and TNF-α production in LPS-treated macrophages. Induction of HO-1 expression increased the level of TTP in the absence of nicotine. In a LPS-induced endotoxemia model, HO-1 deficiency blocked the effects of nicotine on the STAT3 phosphorylation, TTP induction and LPS-induced TNF-α production in the liver. Downregulation of STAT3 by siRNA attenuated the effect of nicotine on TTP exp...
Source: Free Radical Biology and Medicine - October 2, 2013 Category: Biology Authors: Uddin MJ, Joe Y, Zheng M, Blackshear PJ, Ryter SW, Park JW, Chung HT Tags: Free Radic Biol Med Source Type: research

Nicotine potentiates proatherogenic effects of oxLDL by stimulating and upregulating macrophage CD36 signaling
Cigarette smoking is a major risk factor for atherosclerosis and cardiovascular disease. CD36 mediates oxidized LDL (oxLDL) uptake and contributes to macrophage foam cell formation. We investigated a role for the CD36 pathway in nicotine-induced activation of macrophages and foam cell formation in vitro and in vivo. Nicotine in the same plasma concentration range found in smokers increased the CD36+/CD14+ cell population in human peripheral blood mononuclear cells, increased CD36 expression of human THP1 macrophages, and increased macrophage production of reactive oxygen species, PKC phosphorylation, and peroxisome prolife...
Source: AJP: Heart and Circulatory Physiology - August 15, 2013 Category: Cardiology Authors: Zhou, M.-S., Chadipiralla, K., Mendez, A. J., Jaimes, E. A., Silverstein, R. L., Webster, K., Raij, L. Tags: Integrative Cardiovascular Physiology and Pathophysiology Source Type: research

Neutral endopeptidase regulates neurogenic inflammatory responses induced by stimulation of human oral keratinocytes with bacterial lipopolysaccharide and nicotine
In conclusion, the present study demonstrated that NEP down‐regulated the levels of SP and IL‐1β produced from human oral keratinocytes, although ECE‐1 may be partly related to the down‐regulation.
Source: European Journal of Oral Sciences - July 17, 2013 Category: Dentistry Authors: Motoki Nakata, Shuji Awano, Naomasa Kinoshita, Akihiro Yoshida, Toshihiro Ansai Tags: Original Article Source Type: research

Nicotine potentiates oxLDL-induced proatherogenic effects via stimulating and upregulating macrophage CD36 signaling.
Abstract Cigarette smoking is a major risk factor for atherosclerosis and cardiovascular disease. CD36 mediates oxLDL uptake and contributes to macrophage foam cell formation. We investigated a role for the CD36 pathway in nicotine-induced activation of macrophages and foam cell formation in vitro and in vivo. Nicotine in the same plasma concentration range found in smokers increased the CD36(+)/CD14(+) cell population in human peripheral blood mononuclear cells, increased CD36 expression of human THP1 macrophages and increased macrophage production of reactive oxygen species, PKCδ phosphorylation and PPARγ expr...
Source: American Journal of Physiology. Heart and Circulatory Physiology - June 7, 2013 Category: Physiology Authors: Zhou MS, Chadipiralla K, Mendez AJ, Jaimes EA, Silverstein RL, Webster KA, Raij L Tags: Am J Physiol Heart Circ Physiol 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