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Nicotine promotes vascular calcification via intracellular Ca2+-mediated, Nox5-induced oxidative stress and extracellular vesicle release in vascular smooth muscle cells
CONCLUSION: In this study we provide evidence that nicotine induces Nox5-mediated pro-calcific processes as novel mechanism of increased atherosclerotic calcification. We identified that activation of α7 and α3 nAChR by nicotine increases intracellular Ca2+ and initiates calcification of hVSMCs through increased Nox5 activity, leading to oxidative stress-mediated EV release. Identifying the role of Nox5-induced oxidative stress opens novel avenues for diagnosis and treatment of smoking-induced cardiovascular disease.PMID:34273166 | DOI:10.1093/cvr/cvab244
Source: Cell Research - July 17, 2021 Category: Cytology Authors: Ploingarm Petsophonsakul Mathias Burgmaier Brecht Willems Sylvia Heeneman Nadina Stadler Felix Gremse Sebastian Reith Kathrin Burgmaier Florian Kahles Nikolaus Marx Ehsan Natour Elham Bidar Michael Jacobs Barend Mees Chris Reutelingsperger Malgorzata Furm 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

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

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

Nicotine Induced Epithelial-Mesenchymal Transition via Wnt/β-catenin Signaling in Human Airway Epithelial Cells.
Conclusion: These results suggest that HBECs are able to undergo EMT in vitro upon nicotine stimulation via the Wnt3a/β-catenin signaling pathway. PMID: 23204070 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - November 30, 2012 Category: Cytology Authors: Zou W, Zou Y, Zhao Z, Li B, Ran P Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research