VCAM-1 Mediates Cigarette Smoke Extract Enhancement of Monocyte Adhesion to Human Carotid Vascular Endothelial Cells.

Pott, Greg; Tsurudome, Mark; Bui, Jamie; Banfield, Charles; Hourieh, Sami; Pratap, Harsh; Goalstone, Marc L.

doi:10.18103/mra.v5i7.1398

Cited by 4 publications

(4 citation statements)

References 8 publications

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“…We previously demonstrated that HCEC produced significantly greater amounts of mVCAM-1 than mICAM-1 in the presence of CSE in time-and dose-dependent experiments [17]. In the current study, we observed significantly (P < 0.05) increased amounts of mCAMs and sCAMs in the presence of the pro-inflammatory stimuli LPS and TNF (Fig 1 ).…”

Section: Resultssupporting

confidence: 74%

Untitled

2019

RJLBPCS

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Atherosclerosis is a cardiovascular disease that affects the integrity of the arteries and the flow of blood. Indicators of atherosclerosis are, but not limited to, increased expression of Cell Adhesion Molecules (CAMs) on the vascular endothelium, recruitment of serum monocytes (MO) to the endothelium, transmigration of MO across the endothelial layer, maturation of MO to macrophages, plaque formation, and vessel occlusion and rupture. Monocyte adhesion is regulated by the balance between membrane (mCAM) and soluble (sCAMs). We found that Kallikrein-6 (KLK6) cleaves membrane Vascular Cell Adhesion Molecule-1 (mVCAM-1) on vascular endothelial cells, and hypothesized that this proteolytic cleavage event may affect the balance between relative levels of mCAM and sCAM. Since cigarette smoking increases the risk of developing atherosclerosis, we hypothesized that serum extracts of smoke increase the presence of mCAMs and decrease the abundance of sCAMs, thus increasing the likelihood of MO binding to the endothelium. Furthermore, we conjectured that smoking may increase the incidence of plaque formation by affecting an mVCAM-1 protease, leading to decreased sVCAM-1. We determined that in Human Carotid Endothelial Cells (HCEC) (1) Lipopolysaccharide and Tumor Necrosis Factor-alpha increased mVCAM-1 and mICAM-1 (2) cigarette smoke extract (CSE) decreased sVCAM-1, but not sICAM-1, production in timeand dose-dependent manners, (3) KLK6 increased sVCAM-1 and sICAM-1 production in time-and dosedependent manners, (4) aprotinin, a serine protease inhibitor, decreased sVCAM-1, but not sICAM-1, production in a dose-dependent fashion, and (5) KLK6 reversed aprotinin inhibition of sVCAM-1, but not sICAM-1, production.

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Section: Resultssupporting

confidence: 74%

Untitled

2019

RJLBPCS

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“…In previous studies, we noted that expression of total VCAM-1 was not necessarily indicative of expression of VCAM-1 at the cell surface [7,8]. Additionally, since the thrust of these experiments was to define changes in amounts of VCAM-1 protein at the cell surface (i.e., where adhesion to monocytes occurs), we performed only flow cytometry and confocal microscopy experiments and not Western blot analysis.…”

Section: Resultsmentioning

confidence: 99%

Cross talk of c-Jun N-terminal kinase and p38 map kinase modulate insulin and TNFα-stimulated VCAM-1 expression in rat aorta endothelial cells

Pott¹,

Tsurudome²,

Bui³

et al. 2016

ADMET DMPK

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“…We then confirmed these data in healthy non-smoker donor monocytes, with the same results. The existing literature shows conflicting information on the effects of CSE on monocyte migration, with some studies showing increased migration and others decreased migration, which may be due to methods of extraction, cell type, dose, or even different migration assay designs [ 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 ]. There are not any other studies yet investigating the impacts of e-cigarettes on monocyte migration, let alone dual exposure.…”

Section: Discussionmentioning

confidence: 99%

Dual Exposure to E-Cigarette Vapour and Cigarette Smoke Results in Poorer Airway Cell, Monocyte, and Macrophage Function Than Single Exposure

Hamon,

Thredgold,

Wijenayaka

et al. 2024

IJMS

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E-cigarette users predominantly also continue to smoke cigarettes. These Dual Users either consume e-cigarettes in locations where smoking is not allowed, but vaping is, or to reduce their consumption of cigarettes, believing it will lead to harm reduction. Whilst it is known that e-cigarette vapour is chemically less complex than cigarette smoke, it has a distinct chemical profile, and very little is known about the health impacts of exposure to both chemical profiles vs. either alone. We simultaneously exposed cells in vitro to non-toxic levels of e-cigarette vapour extract (EVE) and cigarette smoke extract (CSE) to determine their effects on 16HBE14o- airway epithelial cell metabolism and inflammatory response, as well as immune cell (THP-1 cells and monocyte-derived macrophages (MDM) from healthy volunteers) migration, phagocytosis, and inflammatory response. We observed increased toxicity, reduced metabolism (a marker of proliferation) in airway epithelial cells, and reduced monocyte migration, macrophage phagocytosis, and altered chemokine production after exposure to either CSE or EVE. These cellular responses were greater after dual exposure to CSE and EVE. The airway epithelial cells from smokers showed reduced metabolism after EVE (the Switcher model) and dual CSE and EVE exposure. When EVE and CSE were allowed to interact, the chemicals were found to be altered, and new chemicals were also found compared to the CSE and EVE profiles. Dual exposure to e-cigarette vapour and cigarette smoke led to worse functional outcomes in cells compared to either single exposure alone, adding to limited data that dual use may be more dangerous than smoking only.

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VCAM-1 Mediates Cigarette Smoke Extract Enhancement of Monocyte Adhesion to Human Carotid Vascular Endothelial Cells.

Cited by 4 publications

References 8 publications

Untitled

Untitled

Cross talk of c-Jun N-terminal kinase and p38 map kinase modulate insulin and TNFα-stimulated VCAM-1 expression in rat aorta endothelial cells

Dual Exposure to E-Cigarette Vapour and Cigarette Smoke Results in Poorer Airway Cell, Monocyte, and Macrophage Function Than Single Exposure

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