PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31837232-11 2020 CONCLUSIONS: Across a 24h-period in a hospital setting in the US, nicotine exposure for dual users of e-cigarettes and cigarettes was similar when using cigarettes or variable-power tank devices only but was lower for those using cig-a-like or fixed power devices only. Nicotine 66-74 fibronectin 1 Homo sapiens 104-107 3099825-0 1986 Nicotine alters fibronectin and factor VIII/vWF in human vascular endothelial cells. Nicotine 0-8 fibronectin 1 Homo sapiens 16-27 3099825-8 1986 These studies indicate that nicotine modifies fibronectin and factor VIII/vWF distributions but in different ways. Nicotine 28-36 fibronectin 1 Homo sapiens 46-57 33825493-0 2021 Differential responses to e-cig generated aerosols from humectants and different forms of nicotine in epithelial cells from non-smokers and smokers. Nicotine 90-98 fibronectin 1 Homo sapiens 28-31 33825493-7 2021 We also exposed hNECs from non-smokers and smokers to e-cig generated aerosol from PG:GLY with freebase nicotine or nicotine salt. Nicotine 104-112 fibronectin 1 Homo sapiens 56-59 33825493-7 2021 We also exposed hNECs from non-smokers and smokers to e-cig generated aerosol from PG:GLY with freebase nicotine or nicotine salt. Nicotine 116-124 fibronectin 1 Homo sapiens 56-59 33082140-5 2020 Compared to unexposed controls, nicotine increased NGF, FN1, ET-1, COL1A1, and COL3A1 expression in human and mouse LFs and mouse lung homogenates. Nicotine 32-40 fibronectin 1 Homo sapiens 56-59 34081429-8 2021 For a given PG/VG composition, the addition of nicotine dominated the evaporation dynamics of the e-cig aerosol and the aforementioned negative correlation was no longer observed. Nicotine 47-55 fibronectin 1 Homo sapiens 100-103 33203525-11 2021 CONCLUSIONS: Daily e-cig use may be associated with lower odds of quitting smoking among treatment-seeking smokers, particularly among those with lower nicotine dependence and who initiate daily use after beginning an intervention. Nicotine 152-160 fibronectin 1 Homo sapiens 21-24 31217477-0 2019 Framework to Estimate Total Particulate Mass and Nicotine Delivered to E-cig Users from Natural Environment Monitoring Data. Nicotine 49-57 fibronectin 1 Homo sapiens 73-76 31460462-11 2019 In summary, users of E-cig are exposed to harmful chemicals even if the E-liquids contain only propylene glycol and glycerol without flavorings, nicotine, or impurities. Nicotine 145-153 fibronectin 1 Homo sapiens 23-26 31217477-6 2019 The mass of TPM and nicotine delivered to the mouth of an e-cig user are dependent upon the puffing behavior of the user. Nicotine 20-28 fibronectin 1 Homo sapiens 60-63 26184244-2 2015 However, it has been shown in inexperienced e-cig users that ineffective nicotine delivery can cause tobacco craving that could be responsible for unsuccessful smoking reduction/cessation. Nicotine 73-81 fibronectin 1 Homo sapiens 46-49 30309879-7 2018 Perinatal nicotine exposure resulted in decreased oil red O staining, triolein uptake, expression of PPARgamma, and its downstream target gene adipocyte differentiation-related protein by BMSCs, but enhanced alpha-smooth muscle actin and fibronectin expression, and activated Wnt signaling, all features indicative of their inhibited lipogenic, but enhanced myogenic potential. Nicotine 10-18 fibronectin 1 Homo sapiens 238-249 29572389-9 2018 Similarly, nicotine increased the expression of Wnts, beta-catenin, and fibronectin in normal glucose medium, but further increased mesangial cell expression of these proteins in high glucose milieu. Nicotine 11-19 fibronectin 1 Homo sapiens 72-83 29572389-10 2018 Pharmacological inhibition or genetic knockdown of beta-catenin activity or expression with specific inhibitor FH535 or siRNA significantly impaired the nicotine/glucose-stimulated cell proliferation and fibronectin production. Nicotine 153-161 fibronectin 1 Homo sapiens 204-215 29572389-11 2018 We conclude that nicotine may enhance renal mesangial cell proliferation and fibronectin production under high glucose milieus partly through activating Wnt/beta-catenin pathway. Nicotine 17-25 fibronectin 1 Homo sapiens 77-88 29572389-0 2018 Nicotine enhances mesangial cell proliferation and fibronectin production in high glucose milieu via activation of Wnt/beta-catenin pathway. Nicotine 0-8 fibronectin 1 Homo sapiens 51-62 26184244-3 2015 Moreover, the incorrect use of an e-cig could also led to potential nicotine overdosage and intoxication. Nicotine 68-76 fibronectin 1 Homo sapiens 36-39 26184244-5 2015 We performed an eight-month pilot study of adult smokers who started e-cig use after receiving a multi-component medically assisted training program with monitoring of nicotine intake as a biomarker of correct e-cig use. Nicotine 168-176 fibronectin 1 Homo sapiens 212-215 26184244-9 2015 The proposed medically assisted training program of e-cig use led to a successful nicotine intake, lack of typical cigarette craving and overdosage symptoms and a significant decrease in the biomarker of cigarette combustion products. Nicotine 82-90 fibronectin 1 Homo sapiens 54-57 24809892-5 2014 The cytotoxic components of e-CIG were restrained to the flavoring compound and, to a lesser extent, to nicotine although their effects were less harmful to that of CS. Nicotine 104-112 fibronectin 1 Homo sapiens 30-33 25600647-3 2015 Here, we demonstrate that the scaffolding protein beta-arrestin-1 is necessary for nicotine-mediated induction of mesenchymal genes vimentin and fibronectin as well as EMT regulators ZEB1 and ZEB2. Nicotine 83-91 fibronectin 1 Homo sapiens 145-156 25600647-6 2015 Stimulation of multiple NSCLC cell lines with nicotine led to enhanced recruitment of beta-arrestin-1 and E2F1 on vimentin, fibronectin, and ZEB1 and ZEB2 promoters. Nicotine 46-54 fibronectin 1 Homo sapiens 124-135 24704194-1 2014 The electronic cigarette (e-cig) is a device with a conventional cigarette shape that releases a determined dose of nicotine vapour through an electronic heating process. Nicotine 116-124 fibronectin 1 Homo sapiens 15-18 22489671-11 2012 Nicotine treatment led to the downregulation of ECM molecules, including collagen type I, elastin and fibronectin, and upregulation of MMPs (MMP-1, MMP-2, MMP-8 and MMP-9). Nicotine 0-8 fibronectin 1 Homo sapiens 102-113 23755407-4 2012 Previous investigation indicated that maternal nicotine exposures induce decreased fibronectin expression in lung parenchyma. Nicotine 47-55 fibronectin 1 Homo sapiens 83-94 21944292-0 2011 The effects of nicotine on vascular smooth muscle cell chemotaxis induced by thrombospondin-1 and fibronectin. Nicotine 15-23 fibronectin 1 Homo sapiens 98-109 21944292-3 2011 The hypothesis of this study was that nicotine treatment of vascular cells would augment TSP-1-induced and Fn-induced VSMC migration. Nicotine 38-46 fibronectin 1 Homo sapiens 107-109 21944292-7 2011 Conditioned EC and nicotine-treated conditioned EC enhanced VSMC chemotaxis, which was further augmented by Fn supplementation. Nicotine 19-27 fibronectin 1 Homo sapiens 108-110 21944292-8 2011 CONCLUSIONS: Nicotine-stimulated EC derived factors induce VSMC migration, which is augmented by the addition of Fn. Nicotine 13-21 fibronectin 1 Homo sapiens 113-115 18844224-13 2009 Most importantly, nicotine could induce changes in gene expression consistent with epithelial to mesenchymal transition (EMT), characterized by reduction of epithelial markers like E-cadherin expression, ZO-1 staining and concomitant increase in levels of mesenchymal proteins like vimentin and fibronectin in human breast and lung cancer cells. Nicotine 18-26 fibronectin 1 Homo sapiens 295-306 17600315-8 2007 We then focused on the mechanisms responsible for nicotine-induced fibronectin expression in NSCLC cells and found that nicotine stimulated the surface expression of alpha7 nicotinic acetylcholine receptor (alpha7 nAChR), and that alpha-bungarotoxin, an inhibitor of alpha7 nAChR, abolished the nicotine-induced fibronectin response. Nicotine 50-58 fibronectin 1 Homo sapiens 312-323 17600315-8 2007 We then focused on the mechanisms responsible for nicotine-induced fibronectin expression in NSCLC cells and found that nicotine stimulated the surface expression of alpha7 nicotinic acetylcholine receptor (alpha7 nAChR), and that alpha-bungarotoxin, an inhibitor of alpha7 nAChR, abolished the nicotine-induced fibronectin response. Nicotine 120-128 fibronectin 1 Homo sapiens 67-78 17600315-8 2007 We then focused on the mechanisms responsible for nicotine-induced fibronectin expression in NSCLC cells and found that nicotine stimulated the surface expression of alpha7 nicotinic acetylcholine receptor (alpha7 nAChR), and that alpha-bungarotoxin, an inhibitor of alpha7 nAChR, abolished the nicotine-induced fibronectin response. Nicotine 120-128 fibronectin 1 Homo sapiens 312-323 17600315-8 2007 We then focused on the mechanisms responsible for nicotine-induced fibronectin expression in NSCLC cells and found that nicotine stimulated the surface expression of alpha7 nicotinic acetylcholine receptor (alpha7 nAChR), and that alpha-bungarotoxin, an inhibitor of alpha7 nAChR, abolished the nicotine-induced fibronectin response. Nicotine 120-128 fibronectin 1 Homo sapiens 67-78 17600315-8 2007 We then focused on the mechanisms responsible for nicotine-induced fibronectin expression in NSCLC cells and found that nicotine stimulated the surface expression of alpha7 nicotinic acetylcholine receptor (alpha7 nAChR), and that alpha-bungarotoxin, an inhibitor of alpha7 nAChR, abolished the nicotine-induced fibronectin response. Nicotine 120-128 fibronectin 1 Homo sapiens 312-323 17600315-9 2007 The fibronectin-inducing effects of nicotine were associated with activation of extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3-K)/mammalian target of rapamycin (mTOR) signaling pathways, and were abrogated by inhibitors of ERK (PD98059), PI3-K (LY294002), and mTOR (rapamycin), but not by inhibitors of protein kinase (PK)C (calphostin C) and PKA (H89). Nicotine 36-44 fibronectin 1 Homo sapiens 4-15 17600315-10 2007 These observations suggest that nicotine stimulates NSCLC proliferation through induction of fibronectin, and that these events are mediated through nAChR-mediated signals that include ERK and PI3-K/mTOR pathways. Nicotine 32-40 fibronectin 1 Homo sapiens 93-104 21210228-0 2011 Nicotine enhances colon cancer cell migration by induction of fibronectin. Nicotine 0-8 fibronectin 1 Homo sapiens 62-73 21210228-9 2011 We used inhibitors and siRNA to demonstrate that alpha7-nAChR mediates nicotine-enhanced colon cancer cell migration and upregulates fibronectin expression, which is involved in nicotine-enhanced migration. Nicotine 178-186 fibronectin 1 Homo sapiens 133-144 21210228-10 2011 Furthermore, COX-2 signal was induced by nicotine treatment and is involved in nicotine-enhanced fibronectin expression. Nicotine 41-49 fibronectin 1 Homo sapiens 97-108 21210228-10 2011 Furthermore, COX-2 signal was induced by nicotine treatment and is involved in nicotine-enhanced fibronectin expression. Nicotine 79-87 fibronectin 1 Homo sapiens 97-108 21210228-11 2011 CONCLUSIONS: Nicotine, tobacco"s additive toxin, enhances colon cancer metastasis through alpha7-nAChR and fibronectin--a mesenchymal marker for epithelial mesenchymal transition. Nicotine 13-21 fibronectin 1 Homo sapiens 107-118 17600315-0 2007 Nicotine stimulates human lung cancer cell growth by inducing fibronectin expression. Nicotine 0-8 fibronectin 1 Homo sapiens 62-73 17600315-4 2007 In experiments designed to unveil the mechanisms for this effect, we found that nicotine also stimulated mRNA and protein expression of fibronectin. Nicotine 80-88 fibronectin 1 Homo sapiens 136-147 17600315-7 2007 Thus, nicotine stimulated NSCLC cell proliferation indirectly via fibronectin induction. Nicotine 6-14 fibronectin 1 Homo sapiens 66-77 17600315-8 2007 We then focused on the mechanisms responsible for nicotine-induced fibronectin expression in NSCLC cells and found that nicotine stimulated the surface expression of alpha7 nicotinic acetylcholine receptor (alpha7 nAChR), and that alpha-bungarotoxin, an inhibitor of alpha7 nAChR, abolished the nicotine-induced fibronectin response. Nicotine 50-58 fibronectin 1 Homo sapiens 67-78 16920799-7 2007 At 10 (-7) M, a concentration found in the plasma of active smokers, nicotine induced MC proliferation [control, 1,328 +/- 50 vs. nicotine, 2,761 +/- 90 counts/minute (cpm); P < 0.05] and increased the synthesis of fibronectin (50%), a critical matrix component involved in the progression of chronic kidney disease. Nicotine 69-77 fibronectin 1 Homo sapiens 218-229 15653993-9 2005 Electrophoresis mobility gel shift assays revealed that FP inhibited phosphorylation and DNA binding by the cyclic adenosine monophosphate response element binding protein, a transcription factor required for constitutive and nicotine-induced fibronectin expression. Nicotine 226-234 fibronectin 1 Homo sapiens 243-254