Cigarette smoke extract induces the release of extracellular vesicles by airway epithelial cells via cellular carbonyl stress

Benedikter, Birke J.; Volgers, Charlotte; Haenen, Guido R.M.M.; Savelkoul, Paul H. M.; Wouters, Emiel F.M.; Rohde, Gernot; Weseler, Antje R.; Stassen, Frank R. M.

doi:10.1183/13993003.congress-2015.pa5113

Cited by 4 publications

(5 citation statements)

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“…EVs are released from many different cell types (particularly endothelial cells), and are believed to represent early indicator of cellular changes that lead to chronic disease, including endothelial dysfunction (82). Although we have not identified the source(s) of EVs in our data, plateletsderived EVs have been reported to influence and effect smooth muscle cells (83).…”

Section: Discussionmentioning

confidence: 89%

Long-term cerebrovascular dysfunction in the offspring from maternal electronic cigarette use during pregnancy

Burrage

Aboaziza

Hare

et al. 2021

American Journal of Physiology-Heart and Circulatory Physiology

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Electronic cigarettes (E-cigs) have been promoted as harm-free or less-risky than smoking, even for women during pregnancy. These claims are made largely on E-cig aerosol having fewer number of toxic chemicals compared to cigarette smoke. Given that even low levels of smoking are found to produce adverse birth outcomes, we sought to test the hypothesis that vaping during pregnancy (with or without nicotine) would not be harm-free, and would result in vascular dysfunction that would be evident in offspring during adolescent and/or adult life. Pregnant female Sprague Dawley rats were exposed to E-cig aerosol (1-hour/day, 5 days/week, starting on gestational day 2 until pups were weaned) using e-liquid with 0 mg/ml (E-cig0) or 18 mg/ml nicotine (E-cig18) and compared to ambient air exposed controls. Body mass at birth and at weaning were not different between groups. Assessment of middle cerebral artery (MCA) reactivity revealed a 51-56% reduction in endothelial-dependent dilation response to acetylcholine (ACh) for both E-cig0 and E-cig18 in 1-month, 3-month (adolescent), and 7-month old (adult) offspring (p<0.05 compared to air, all time points). MCA response to sodium nitroprusside (SNP) and myogenic tone were not different across groups suggesting that endothelial-independent responses were not altered. The MCA vasoconstrictor response (5-hydroxytryptamine, 5-HT) was also not different across treatment and age groups. These data demonstrate that maternal vaping during pregnancy is not harm-free and confers significant cerebrovascular health risk/dysfunction to offspring that persists into adult life.

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Section: Discussionmentioning

confidence: 89%

Long-term cerebrovascular dysfunction in the offspring from maternal electronic cigarette use during pregnancy

Burrage

Aboaziza

Hare

et al. 2021

American Journal of Physiology-Heart and Circulatory Physiology

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“…Benedikter et al . found that CSE can induce a 2.3-fold increase in the release of extracellular vesicles (EVs) from airway epithelial cells [ 36 ]. Furthermore, both the lipid profile of the EV membrane and the protein profile inside EV undergo significant changes with CSE exposure [ 37 , 38 ].…”

Section: Resultsmentioning

confidence: 99%

Targeting CCL2-CCR2 signaling pathway alleviates macrophage dysfunction in COPD via PI3K-AKT axis

Dong,

Zhu

et al. 2024

Cell Commun Signal

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Background Chronic obstructive pulmonary disease (COPD) remains a leading cause of morbidity and mortality worldwide, characterized by persistent respiratory symptoms and airflow limitation. The involvement of C–C motif chemokine ligand 2 (CCL2) in COPD pathogenesis, particularly in macrophage regulation and activation, is poorly understood despite its recognized role in chronic inflammation. Our study aims to elucidate the regulatory role and molecular mechanisms of CCL2 in the pathogenesis of COPD, providing new insights for therapeutic strategies. Methods This study focused on the CCL2-CCR2 signaling pathway, exploring its role in COPD pathogenesis using both Ccl2 knockout (KO) mice and pharmacological inhibitors. To dissect the underlying mechanisms, we employed various in vitro and in vivo methods to analyze the secretion patterns and pathogenic effects of CCL2 and its downstream molecular signaling through the CCL2-CCR2 axis. Results Elevated Ccl2 expression was confirmed in the lungs of COPD mice and was associated with enhanced recruitment and activation of macrophages. Deletion of Ccl2 in knockout mice, as well as treatment with a Ccr2 inhibitor, resulted in protection against CS- and LPS-induced alveolar injury and airway remodeling. Mechanistically, CCL2 was predominantly secreted by bronchial epithelial cells in a process dependent on STAT1 phosphorylation and acted through the CCR2 receptor on macrophages. This interaction activated the PI3K-AKT signaling pathway, which was pivotal for macrophage activation and the secretion of inflammatory cytokines, further influencing the progression of COPD. Conclusions The study highlighted the crucial role of CCL2 in mediating inflammatory responses and remodeling in COPD. It enhanced our understanding of COPD's molecular mechanisms, particularly how CCL2's interaction with the CCR2 activates critical signaling pathways. Targeting the CCL2-CCR2 axis emerged as a promising strategy to alleviate COPD pathology. Graphical Abstract

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“…The EV concentration relative to the dead cells then increased further on bioprocess day 9, just before the increasing cell death (i.e. days 10,11,12). Therefore, this increase in EV concentration was not just the result of cells dying, but was the result of EV-budding processes that were triggered by the stress conditions.…”

Section: Concentration Of Extracellular Vesicles As a New Parameter Fmentioning

confidence: 97%

“…Vesicles can be released into their microenvironment continuously, or they can be released according to the diverse physiological conditions of the system [5,7]. Indeed, they are rapidly released by cells during cell activation, such as during mechanical [8] and oxidative stress [9], carbonyl stress [10], and elevated intracellular Ca 2+ levels [11,12], during temperature elevation through physical exercise or exposure to external heat [13,14], and during exposure to low temperatures [15]. Such conditions can result in a significant increase in vesicle numbers in blood samples or cell culture supernatants.…”

mentioning

confidence: 99%

Extracellular vesicles concentration is a promising and important parameter for industrial bioprocess monitoring

Zavec

Kralj‐Iglič

Brinc³

et al. 2016

Biotechnology Journal

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Extracellular vesicles (EVs) are membrane vesicles that are produced by cells to be released into their microenvironment. In this study, we present the EV concentration as a new factor for optimization of industrial bioprocess control. The release of EVs depends on many cell properties, including cell activation and stress status, and cell death. Therefore, the EV concentration might provide a readout for identification of the cell state and the conditions during a bioprocess. Our data show that the EV concentration increased during the bioprocess, which indicated deteriorating conditions in the bioreactor. This increase in EV concentration in the fermentation broth was the consequence of two different processes: cell activation, and cell death. However, the release of EVs from activated living cells had a much weaker impact on EV concentration in the bioreactor than those released during cell death. EVs and cells in the bioprocess environment were quantified by flow cytometry. The most accurate data were obtained directly from unprocessed samples, making the monitoring of the EV concentration a rapid, easy, and cheap method. These EV concentrations reflect the conditions in the bioreactor and provide new information regarding the state of the bioprocess. Therefore, we suggest EV concentration as a new and important parameter for the monitoring of industrial bioprocesses.

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Cigarette smoke extract induces the release of extracellular vesicles by airway epithelial cells via cellular carbonyl stress

Cited by 4 publications

References 0 publications

Long-term cerebrovascular dysfunction in the offspring from maternal electronic cigarette use during pregnancy

Long-term cerebrovascular dysfunction in the offspring from maternal electronic cigarette use during pregnancy

Targeting CCL2-CCR2 signaling pathway alleviates macrophage dysfunction in COPD via PI3K-AKT axis

Extracellular vesicles concentration is a promising and important parameter for industrial bioprocess monitoring

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