CCN1 secretion and cleavage regulate the lung epithelial cell functions after cigarette smoke

Moon, Hyung‐Geun; Kim, Sang Heon; Gao, Jinming; Quan, Taihao; Qin, Zhaoping; Osorio, Juan C.; Rosas, Iván O.; Wu, Min; Tesfaigzi, Yohannes; Jin, Yang

doi:10.1152/ajplung.00102.2014

Cited by 98 publications

(101 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Chen et al (2016) demonstrated that EV from CSEexposed macrophages contain the pro-inflammatory alarmin high-mobility group box 1. Further, EV from CSE-exposed macrophages and epithelial cells, as well as EV isolated from BALF of smokers trigger release of interleukin-(IL-) 6, IL-8, and monocyte chemoattractant protein 1 (MCP1) by naïve pulmonary epithelial cells (Cordazzo et al 2014;Héliot et al 2017;Moon et al 2014). EV also promote upregulation of intercellular adhesion molecule 1 (Cordazzo et al 2014) and thus may contribute to inflammation and immune cell recruitment toward EV target cells.…”

Section: Promotion Of Pro-inflammatory Signalingmentioning

confidence: 99%

“…The studies that report either induction (Cordazzo et al 2014;Héliot et al 2017;Moon et al 2014) or no induction ) of pro-inflammatory cytokines by CS(E)-induced EV in vitro have all employed similar exposure times, EV isolation techniques, and EV target cells (bronchial epithelial cells). Yet, the divergent results might be explained by the quantity of EV used in functional assays as Héliot et al (2017) obtained their positive results with 100-fold more EV than the quantity that resulted in negative results .…”

Section: Conflicting Datamentioning

confidence: 99%

“…Folkesson et al (2015) found that, when exposed to CSE, neutrophil-like HL60 cells secreted EV-associated and proteolytically active a disintegrin and metalloproteinase (ADAM)10 and ADAM17. Finally, EV released by lung epithelial cells in response to CSE promoted production of MMP1 by EV target cells (Moon et al 2014). Xu and Deng (2004) demonstrated that CS-induced secretion of EV-bound proteolytic calpains was associated with increased migration and invasiveness of the EV-secreting lung carcinoma cells.…”

Section: Extracellular Vesicles-associated Proteolytic Enzymesmentioning

confidence: 99%

“…Further, EV from CSEtreated lung epithelial cells promote secretion of the proangiogenic vascular endothelial growth factor (VEGF) by EV target cells (Liu et al 2014;Moon et al 2014). Liu et al (2014) demonstrated that VEGF induction was mediated by EV-associated microRNA-21 and was able to trigger endothelial tube formation.…”

Section: Respiratory Exposure-induced Extracellular Vesicles and Angimentioning

confidence: 99%

See 3 more Smart Citations

Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

Benedikter

Wouters

Savelkoul

et al. 2018

Journal of Toxicology and Environmental Health, Part B

View full text Add to dashboard Cite

Extracellular vesicles (EV) are secreted signaling entities that enhance various pathological processes when released in response to cellular stresses. Respiratory exposures such as cigarette smoke and air pollution exert cellular stresses and are associated with an increased risk of several chronic diseases. The aim of this review was to examine the evidence that modifications in EV contribute to respiratory exposure-associated diseases. Publications were searched using PubMed and Google Scholar with the search terms (cigarette smoke OR tobacco smoke OR air pollution OR particulate matter) AND (extracellular vesicles OR exosomes OR microvesicles OR microparticles OR ectosomes). All original research articles were included and reviewed. Fifty articles were identified, most of which investigated the effect of respiratory exposures on EV release in vitro (25) and/or on circulating EV in human plasma (24). The majority of studies based their main observations on the relatively insensitive scatter-based flow cytometry of EV (29). EV induced by respiratory exposures were found to modulate inflammation (19), thrombosis (13), endothelial dysfunction (11), tissue remodeling (6), and angiogenesis (3). By influencing these processes, EV may play a key role in the development of cardiovascular diseases and chronic obstructive pulmonary disease and possibly lung cancer and allergic asthma. The current findings warrant additional research with improved methodologies to evaluate the contribution of respiratory exposure-induced EV to disease etiology, as well as their potential as biomarkers of exposure or risk and as novel targets for preventive or therapeutic strategies.

show abstract

Section: Promotion Of Pro-inflammatory Signalingmentioning

confidence: 99%

Section: Conflicting Datamentioning

confidence: 99%

Section: Extracellular Vesicles-associated Proteolytic Enzymesmentioning

confidence: 99%

Section: Respiratory Exposure-induced Extracellular Vesicles and Angimentioning

confidence: 99%

See 2 more Smart Citations

Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

Benedikter

Wouters

Savelkoul

et al. 2018

Journal of Toxicology and Environmental Health, Part B

View full text Add to dashboard Cite

show abstract

“…Since the authors suggest that the measured weight reduction and increased mortality are due to an increase of lung injury, it would be further necessary to analyze whether the lung morphology was phenotypically altered and whether the measured increase in bronchoalveolar lavage fluid neutrophil counts impacts the total content of immune cells infiltrating the lung. It is quite possible that the weight loss is simply due to CCN1-induced promotion of epithelial cell death and tissue loss that was previously found in mice with emphyseamatous changes after prolonged cigarette smoke exposure (8). All these issues would be worth to be analyzed in future studies to understand the pathophysiological role of CCN1 in injured lung tissue.…”

mentioning

confidence: 93%

Ccn1, a molecular switch that imposes a self-limiting control on inflammation and wound healing in a multitude of organs?

Weiskirchen

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

Extracellular vesicles in toxicological studies: key roles in communication between environmental stress and adverse outcomes

Qin

Huang

2020

J of Applied Toxicology

View full text Add to dashboard Cite

External stressors, especially environmental toxicants can disturb biological homeostasis and thus lead to adverse health effects. However, there is limited understanding of how cells directly exposed to stressors transmit the signals to cells indirectly in contact with stressors. Extracellular vesicles (EVs) are receiving increasing attention as signal transductors between various types of cells in organisms. Cargo in EVs, including RNAs, proteins, lipids, and other signal molecules can be transferred between cells and become critical determining factors of intercellular communication. EVs can be a powerful mediator of environmental stimuli. It has been shown that external stressors reshape the secretion of EVs, modify the composition of EVs, and thus influence the mediating function of EVs. These abnormal EVs can lead to dysfunction of recipient cells, and even the pathogenesis of diseases. In this review, we first summarized current knowledge about the responses of EVs to external stimuli, including chemicals and chemical mixtures. Then we explained how these altered EVs regulate signal pathways in recipient cells, thus mediating physio‐pathological responses in detail. The most up‐to‐date evidence from molecular, cellular, animal and human levels was synthesized to systematically address the mediating roles of EVs. EVs can be regarded as a bridge to link external stressors and internal response. Further toxicological and molecular epidemiological studies are expected to provide further insight into the roles of EVs in toxicology. The gaps in the engulfment of toxicants into EVs are listed as the priority to be solved in future studies.

show abstract

CCN1 secretion and cleavage regulate the lung epithelial cell functions after cigarette smoke

Abstract: . CCN1 secretion and cleavage regulate the lung epithelial cell functions after cigarette smoke.

Cited by 98 publications

References 46 publications

Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

Ccn1, a molecular switch that imposes a self-limiting control on inflammation and wound healing in a multitude of organs?

Extracellular vesicles in toxicological studies: key roles in communication between environmental stress and adverse outcomes

Contact Info

Product

Resources

About