Nicotine could augment adhesion molecule expression in human endothelial cells through macrophages secreting TNF-α, IL-1β

Wang, Yajing; Wang, Lianyun; Ai, Xinghao; Zhao, Jianli; Xia, Hao; Lu, Yutong; Qiao, Zhongdong

doi:10.1016/j.intimp.2004.07.028

Cited by 62 publications

(34 citation statements)

References 29 publications

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“…Contradictory effects of nicotine are reported in the literature, since some authors demonstrated detrimental activities while others suggested a beneficial effect. Lau et al (2006) documented a 2.5-fold larger atherosclerotic lesion in nicotine-treated than placebo-treated mice, and nicotine was demonstrated to enhance adhesion molecule expression in human endothelial cells through macrophages releasing TNF-α and IL-1β (Wang et al, 2004). In immortalized cell lines, nicotine-induced apoptosis, increased oxidative stress and activated NF-κB (Crowley-Weber et al, 2003;Wu et al, 2002).…”

Section: Discussionmentioning

confidence: 97%

Quantification of PPAR-γ protein in monocyte/macrophages from healthy smokers and non-smokers: A possible direct effect of nicotine

et al. 2007

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Section: Discussionmentioning

confidence: 97%

Quantification of PPAR-γ protein in monocyte/macrophages from healthy smokers and non-smokers: A possible direct effect of nicotine

et al. 2007

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“…Recombinant sVCAM-1, sE-selectin was used to establish a standard curve. HUVECs (10 7 cells/dish) were activated with 60 μM nicotine as described previously [13]. Cells were stimulated for 15 min with 60 μM nicotine or co-treated with 100 nM E 2 .…”

Section: Determination Of Svcam-1 Se-selectin By Elisamentioning

confidence: 99%

Estrogen down-regulates nicotine-induced adhesion molecule expression via nongenomic signal pathway in endothelial cells

Wang

et al. 2006

International Immunopharmacology

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“…Prior in vitro studies have shown that high concentrations of cigarette smoke extract 6,28,29 and nicotine [32][33][34] increase adhesion molecule expression on ECs. These studies preclude the involvement of physiological shear stresses.…”

Section: Introductionmentioning

confidence: 99%

In Vitro Model of Platelet-Endothelial Activation Due to Cigarette Smoke Under Cardiovascular Circulation Conditions

Girdhar

Jesty

et al. 2008

Ann Biomed Eng

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Cigarette smoke has been shown to increase platelet activation and endothelial cell (EC) adhesion molecule expression. In the present study, we utilized a hemodynamic shearing device (HSD) to investigate the above effects in vitro in a combined system of platelets and cultured HUVECs (Human Umblical Vein ECs) under physiological shear stress. We investigated the alteration of E-selectin expression on ECs upon exposure to: (1) platelets and nicotine-free smoke extract (NFE), (2) platelets alone, (3) NFE alone, under physiological shear stress. We additionally confirmed the protective effect of nicotine on platelet activation. We found that: (i) surface expression of E-selectin on ECs was significantly increased upon simultaneous exposure of ECs and platelets to NFE relative to exposure of ECs to either platelets or NFE alone (p < 0.05). (ii) Platelet activation was significantly increased in the presence of NFE (p < 0.05). (iii) Nicotine (200 nM) when added to NFE, significantly reduced platelet activation due to NFE (p < 0.05), an effect additionally confirmed by conventional cigarette extracts which contain nicotine (p < 0.05). We therefore conclude that: (a) NFE and platelets additively increase EC E-selectin surface expression, and (b) nicotine modulates platelet activation regardless of ECs.

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Nicotine could augment adhesion molecule expression in human endothelial cells through macrophages secreting TNF-α, IL-1β

Cited by 62 publications

References 29 publications

Quantification of PPAR-γ protein in monocyte/macrophages from healthy smokers and non-smokers: A possible direct effect of nicotine

Quantification of PPAR-γ protein in monocyte/macrophages from healthy smokers and non-smokers: A possible direct effect of nicotine

Estrogen down-regulates nicotine-induced adhesion molecule expression via nongenomic signal pathway in endothelial cells

In Vitro Model of Platelet-Endothelial Activation Due to Cigarette Smoke Under Cardiovascular Circulation Conditions

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