Effect of nicotine on human umbilical vein endothelial cells (HUVECs) migration and angiogenesis

Park, Yang Jin; Lee, Taeseung; Ha, Jongwon; Jung, In Mok; Chung, Jung Kee; Kim, Sang Joon

doi:10.1016/j.vph.2008.05.001

Cited by 33 publications

(30 citation statements)

References 21 publications

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“…Consistent with previous studies [5,16,29], the results from our study indicated that not only NT, but also nornicotine effectively disrupts the balance of VEGF and PEDF, resulting in an increased VEGF/PEDF mRNA ratio in ARPE-19 cells as well as in HUVECs in a dose- and time- dependent manner.…”

Section: Discussionsupporting

confidence: 92%

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Nornicotine and Nicotine Induced Neovascularization via Increased VEGF/PEDF Ratio

Zhang¹,

Wang³

et al. 2015

Ophthalmic Res

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Purpose: The purpose of the current study was to evaluate the influences of nornicotine and nicotine (NT) in cigarette smoke on the expression of vascular endothelial growth factor (VEGF) and pigment epithelium-derived factor (PEDF) in retinal pigment epithelium cells and human umbilical vein endothelial cells (HUVECs). Furthermore, the angiogenic behaviors of endothelial cells under nornicotine and NT treatment were assessed by using in vitro methods. Methods: ARPE-19 cells and HUVECs were treated with different concentrations of either nornicotine or NT for different periods of time. The cell proliferative effect was investigated by using the method of MTT analysis. HUVEC migration and tube formation were assessed by using the scratch assay and Matrigel models. The expressions of VEGF and PEDF gene and protein in both types of cells were examined by real-time RT-PCR and Western blot. Results: There was no proliferation of ARPE-19 cells following treatment with various concentrations of nornicotine or NT. In contrast, nornicotine or NT significantly stimulated HUVEC proliferation, migration and tube formation. Nornicotine and NT upregulated the expression of VEGF but suppressed the expression of PEDF at both mRNA and protein levels in a dose- and time-dependent manner in ARPE-19 cells and HUVECs. Conclusions: Our results demonstrate that nornicotine and NT promoted endothelial cellular proliferation, migration and tube formation of HUVECs in vitro. These effects might be partly due to simultaneous modulation of VEGF/PEDF signaling in ARPE-19 cells and HUVECs.

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Section: Discussionsupporting

confidence: 92%

“…NT exerts its biological effects through binding to nicotinic cholinergic receptors [14,15]. NT has been shown to be mitogenic for endothelial cells, to induce cell proliferation and tube formation [16,17]. …”

Section: Introductionmentioning

confidence: 99%

Nornicotine and Nicotine Induced Neovascularization via Increased VEGF/PEDF Ratio

Zhang¹,

Wang³

et al. 2015

Ophthalmic Res

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“…This result suggests that nicotine could promote pro-inflammatory response in endothelial cells. This is consistent with Park's report that acrolein, another toxicant in cigarette smoke induced COX-2 and PGE 2 expression in HUVECs [28].…”

Section: Discussionsupporting

confidence: 93%

Nicotine induces cyclooxygenase-2 and prostaglandin E2 expression in human umbilical vein endothelial cells

Zhou

Wang

Tang

et al. 2010

International Immunopharmacology

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“…The effects of both of these compounds on the cells used in this study are complex and not well defined. In fact, a previous study found that at concentrations typically found in the blood of smokers, the effects of nicotine on endothelial migration in vitro were in fact stimulatory (Park et al, 2008), which conflicts with the inhibition of migration seen in our study. Therefore further studies may be required to define the sensitivity of the migration assay to both nicotine and cotinine.…”

Section: Proteincontrasting

confidence: 99%

Examination of the use of human sera as an exposure agent for in vitro studies investigating the effects of cigarette smoking on cellular cardiovascular disease models

McQuillan

Carr

Taylor

et al. 2015

Toxicology in Vitro

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In vitro models of smoking-related diseases and disease processes are valuable for mechanistic understanding and assessment of novel tobacco products. Many laboratories have used particulate phase or aqueous extracts of cigarette smoke as an exposure system for in vitro models. However, this may not be the most relevant method of exposing cells to smoke and its toxicants. Here we have examined the use of human serum as an exposure system. Cultured human umbilical vein endothelial cells were exposed in vitro to sera (50% dilution in culture media) from human volunteers (9 smokers; 10 non-smokers) for 20 h. Statistically-significant differential changes were detected in endothelial migration in an endothelial damage repair model, such that smokers' sera had an inhibitory effect on migration compared with sera from non-smokers (p<0.05). We further observed several statistically-significant differences in cardiovascular disease (CVD)-relevant gene expression between cells exposed to smokers' and non-smokers' sera, as well as differences in levels of cytokines secreted from endothelial cells. Our data demonstrate that human sera from smokers and non-smokers can differentially regulate endothelial function. We suggest that human serum provides a relevant exposure medium for in vitro studies assessing the impact of cigarette smoking on CVD risk potential.

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Effect of nicotine on human umbilical vein endothelial cells (HUVECs) migration and angiogenesis

Cited by 33 publications

References 21 publications

Nornicotine and Nicotine Induced Neovascularization via Increased VEGF/PEDF Ratio

Nornicotine and Nicotine Induced Neovascularization via Increased VEGF/PEDF Ratio

Nicotine induces cyclooxygenase-2 and prostaglandin E2 expression in human umbilical vein endothelial cells

Examination of the use of human sera as an exposure agent for in vitro studies investigating the effects of cigarette smoking on cellular cardiovascular disease models

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