| Name | VEGF |
|---|---|
| Synonyms | VEGF; VEGF A; VEGFA; VPF; Vascular endothelial growth factor A; Vascular endothelial growth factor A precursor; Vascular permeability factor; vascular endothelial growth factor… |
| Name | nicotine |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 19501920 | Huang H, Lavoie-Lamoureux A, Lavoie JP: Cholinergic stimulation attenuates the IL-4 induced expression of E-selectin and vascular endothelial growth factor by equine pulmonary artery endothelial cells. Vet Immunol Immunopathol. 2009 Dec 15;132(2-4):116-21. Epub 2009 May 18. Using primary equine pulmonary artery endothelial cells culture and real-time RT-PCR method, we observed that nicotine, and muscarine inhibit the expression of E-selectin and vascular endothelial growth factor by endothelial cells stimulated by reIL-4. |
82(1,1,1,2) | Details |
| 19896492 | Oloris SC, Frazer-Abel AA, Jubala CM, Fosmire SP, Helm KM, Robinson SR, Korpela DM, Duckett MM, Baksh S, Modiano JF: Nicotine-mediated signals modulate cell death and survival of T lymphocytes. Toxicol Appl Pharmacol. 2010 Feb 1;242(3):299-309. Epub 2009 Nov 4. Previously, we showed that exposure to nicotine activates the nuclear factor of activated T cells (NFAT) transcription factor in lymphocytes and endothelial cells, leading to alterations in cellular growth and vascular endothelial growth factor production. |
81(1,1,1,1) | Details |
| 20223446 | Mimura K, Tomimatsu T, Sharentuya N, Tskitishvili E, Kinugasa-Taniguchi Y, Kanagawa T, Kimura T: Nicotine restores endothelial dysfunction caused by excess sFlt1 and sEng in an in vitro model of preeclamptic vascular endothelium: a possible therapeutic role of nicotinic acetylcholine receptor (nAChR) agonists for preeclampsia. Am J Obstet Gynecol. 2010 Mar 10. Enzyme-linked immunosorbent assay was performed to measure vascular endothelial growth factor, placental growth factor, and transforming growth factor-beta1 concentrations in the conditioned media treated with nicotine (10 (-9) to 10 (-6) M). |
32(0,1,1,2) | Details |
| 19778953 | Konishi H, Wu J, Cooke JP: Chronic exposure to nicotine impairs cholinergic angiogenesis. Vasc Med. 2010 Feb;15(1):47-54. Epub 2009 Sep 24. In conclusion, the current study shows for the first time that chronic exposure to nicotine impairs cholinergic angiogenesis, an effect mediated by downregulation of the vascular nAChR, and attenuation of nicotine-induced VEGF release. |
32(0,1,1,2) | Details |
| 20200934 | Ma L, Zheng LW, Sham MH, Cheung LK: Uncoupled angiogenesis and osteogenesis in nicotine compromised bone healing. J Bone Miner Res. 2010 Jan 14. Nicotine exposure upregulated the expression of hypoxia inducible factor 1alpha and vascular endothelial growth factor and enhanced angiogenesis, but inhibited the expression of bone morphogenetic protein-2 and impaired bone healing. |
31(0,1,1,1) | Details |
| 19962381 | Kakinuma Y, Furihata M, Akiyama T, Arikawa M, Handa T, Katare RG, Sato T: an acetylcholinesterase inhibitor against Alzheimer's dementia, promotes angiogenesis in an ischemic hindlimb model. J Mol Cell Cardiol. 2010 Apr;48(4):680-93. Epub 2009 Dec 3. Our recent studies have indicated that protects cardiomyocytes from prolonged hypoxia through activation of the PI3K/Akt/HIF-1alpha/VEGF pathway and that cardiomyocyte-derived VEGF promotes angiogenesis in a paracrine fashion. and nicotine upregulated signal transduction with acceleration of tube formation, suggesting that promotes a common angiogenesis pathway. |
4(0,0,0,4) | Details |
| 19305373 | De Luca L, De Angelis C, Fagoonee S, Di Bella S, Rizzetto M, Pellicano R: Is smoking a prognostic factor in patients with chronic hepatitis C? . Minerva Gastroenterol Dietol. 2009 Jun;55(2):139-43. Nicotine is mainly metabolised by the liver, and its administration in experimental animals showed development of steatosis and focal or confluent hepatic necrosis, probably linked to the oxidative stress associated with lipid peroxidation. In chronic hepatitis C patients, preliminary studies have suggested that hypoxia caused by smoking may induce expression of the cytokines vascular endothelial growth factor (VEGF) and VEGF-D and their corresponding soluble tyrosine kinase receptors fms-like tyrosine kinase receptor and kinase insert domain receptor. |
1(0,0,0,1) | Details |
| 19387337 | Al-Wadei HA, Al-Wadei MH, Schuller HM: Prevention of pancreatic cancer by the beta-blocker . Anticancer Drugs. 2009 Jul;20(6):477-82. We have previously reported that beta-adrenergic receptors (beta-ARs) stimulate the proliferation and migration of human PDAC cells in vitro by cAMP-dependent signaling and that the nicotine-derived nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1- (NNK) activates this pathway directly in vitro while additionally stimulating the release of / by binding to alpha7 nicotinic acetylcholine receptors (alpha7 nAChR) in hamsters. Our data suggest that may prevent the development of PDAC by blocking cAMP-dependent intracellular signaling, cAMP-dependent release of epidermal growth factor, and PKA-dependent release of vascular endothelial growth factor while additionally downregulating the alpha7 nAChR by inhibiting cAMP-mediated subunit assembly. |
1(0,0,0,1) | Details |
| 19536709 | Herr F, Baal N, Zygmunt M: Studies of placental vasculogenesis: a way to understand pregnancy pathology?. Z Geburtshilfe Neonatol. 2009 Jun;213(3):96-100. Epub 2009 Jun 17. VEGF, bFGF) as well as pregnancy specific (PlGF, hCG, IGF-II, AFP) angiogenic factors are involved. Pregnancy-associated exposure to bacterial and viral infections or toxic agents (e. g. nicotine or drugs) may also influence vascular development of the placenta and often lead to preterm labour and delivery. |
1(0,0,0,1) | Details |
| 19326440 | Paleari L, Sessa F, Catassi A, Servent D, Mourier G, Doria-Miglietta G, Ognio E, Cilli M, Dominioni L, Paolucci M, Calcaterra A, Cesario A, Margaritora S, Granone P, Russo P: Inhibition of non-neuronal alpha7-nicotinic receptor reduces tumorigenicity in A549 NSCLC xenografts. Int J Cancer. 2009 Jul 1;125(1):199-211. Nicotine (classical nAChR agonist) induced cell proliferation, whereas nAChR antagonists, d- tubocurarine or alpha-cobratoxin (alpha-CbT), induced cell death. Moreover, neoangiogenesis was strongly inhibited (reduction of cells positive to vascular endothelial growth factor and CD31). |
1(0,0,0,1) | Details |
| 19693712 | Petrik JJ, Gerstein HC, Cesta CE, Kellenberger LD, Alfaidy N, Holloway AC: Effects of on ovarian function and fertility in animals with reduced fertility following fetal and neonatal exposure to nicotine. Endocrine. 2009 Oct;36(2):281-90. Epub 2009 Aug 20. Moreover, ovaries from NV animals had decreased levels of the pro-angiogenic growth factors vascular endothelial growth factor (VEGF) and endocrine gland-derived VEGF both of which were increased with treatment. |
1(0,0,0,1) | Details |