In vitro short-term exposure to air pollution PM2.5-0.3 induced cell cycle alterations and genetic instability in a human lung cell coculture model

Abbas, Imane; Verdin, Anthony; Escande, Fabienne; Saint-Georges, Françoise; Cazier, Fabrice; Mulliez, P.; Courcot, Dominique; Shirali, Pirouz; Gosset, Pierre; Garçon, Guillaume

doi:10.1016/j.envres.2016.01.041

Cited by 53 publications

(23 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It also significantly induced oxidative damage, DNA strand breaks, and apoptosis by the p53-dependent pathway [ 57 ]. PM 2.5–0.3 induces genetic instability and alterations of the cell cycle via TP53-RB gene signaling pathway activation in human alveolar macrophages and an L132 co-culture model [ 59 ]. Industrial PM 2.5 extracts enhance inflammation and pulmonary epithelial cell injuries via the RhoA/ROCK-dependent NF-кB signaling pathway in a co-culture system of BEAS-2 and THP-1 cells [ 60 ].…”

Section: In Vitro Experimental Studies Of Pm 25 mentioning

confidence: 99%

In Vitro and In Vivo Experimental Studies of PM2.5 on Disease Progression

Cho

Hsieh

Tsai

et al. 2018

IJERPH

149

View full text Add to dashboard Cite

Air pollution is a very critical issue worldwide, particularly in developing countries. Particulate matter (PM) is a type of air pollution that comprises a heterogeneous mixture of different particle sizes and chemical compositions. There are various sources of fine PM (PM2.5), and the components may also have different effects on people. The pathogenesis of PM2.5 in several diseases remains to be clarified. There is a long history of epidemiological research on PM2.5 in several diseases. Numerous studies show that PM2.5 can induce a variety of chronic diseases, such as respiratory system damage, cardiovascular dysfunction, and diabetes mellitus. However, the epidemiological evidence associated with potential mechanisms in the progression of diseases need to be proved precisely through in vitro and in vivo investigations. Suggested mechanisms of PM2.5 that lead to adverse effects and chronic diseases include increasing oxidative stress, inflammatory responses, and genotoxicity. The aim of this review is to provide a brief overview of in vitro and in vivo experimental studies of PM2.5 in the progression of various diseases from the last decade. The summarized research results could provide clear information about the mechanisms and progression of PM2.5-induced disease.

show abstract

Section: In Vitro Experimental Studies Of Pm 25 mentioning

confidence: 99%

In Vitro and In Vivo Experimental Studies of PM2.5 on Disease Progression

Cho

Hsieh

Tsai

et al. 2018

IJERPH

149

View full text Add to dashboard Cite

show abstract

“…DNA damage, cell apoptosis, cell necrosis, autophagy and cell abnormalities have been identified to occur during PM2.5-induced cytotoxicity (10)(11)(12). Although a number of reports have attempted to understand PM2.5-induced lung injury, the underlying processes and signaling mechanisms governing the effect of PM2.5 on the lungs have not yet been clearly elucidated (13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

PM2.5 induces autophagy‑mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells

Han

Zhuang

2020

Exp Ther Med

View full text Add to dashboard Cite

Air pollution can highly impact the respiratory system in healthy individuals. Studies have indicated that particles with an aerodynamic diameter of ≤2.5 µm (PM2.5) can be considered to be harmful for lung alveoli and bronchial epithelium cells. PM2.5 can be directly inhaled and can deeply penetrate into the lung alveoli, causing lung dysfunction. However, the toxicological mechanism mediated by PM2.5 for respiratory disease has still not been clearly determined. The purpose of the current study was to investigate the effects of PM2.5 on mouse bronchial epithelium cells (MBECs) and explored the possible mechanism mediated by PM2.5 in MBECs. The results of the current study indicated that PM2.5 markedly decreased lung function, including total lung capacity, residual volume, vital capacity and airway resistance in experimental mice. The results demonstrated that PM2.5 markedly induced inflammatory responses, oxidative injury and MBEC apoptosis. PM2.5 increased interleukin (IL)-1β and IL-6 expression, and reactive oxygen species production in MBECs. Furthermore, PM2.5 specifically induced PI3K, AKT and mTOR expression in MBECs. Disruption of PI3K/AKT/mTOR signaling was also indicated to effectively inhibit apoptosis of MBECs. In conclusion, the results of the current study systematically demonstrated the role of apoptosis-mediated MBEC apoptosis in PM2.5-treated mice, and provides a potential strategy for preclinical intervention in patients with PM2.5-induced lung diseases.

show abstract

“…19 It was demonstrated that PM 2.5 exposure induced cell cycle arrest at the G1/S or G2/M phase. 20,21 As shown in Table 2 and Fig. 3A, both FBC and OBC could induce significant cell cycle arrest at the S phase.…”

Section: Cell Cycle Arrest Induced By Fbc and Obc Treatmentmentioning

confidence: 86%

“…FBC and OBC were sonicated in a microtherm and then diluted with F-12 HAM'S medium. Based on preliminary experiments (concentrations ranging from 1 to 100 μg mL −1 , data not shown), three concentrations (10,20, and 40 μg mL −1 ) of FBC and OBC with mild to moderate mortality were selected for this study. In the treatment groups, A549 cells were co-incubated with FBC or OBC at different times.…”

Section: Cell Culturementioning

confidence: 99%

Fresh and ozonized black carbon promoted DNA damage and repair responses in A549 cells

Wang

et al. 2019

Toxicol. Res.

View full text Add to dashboard Cite

show abstract

In vitro short-term exposure to air pollution PM2.5-0.3 induced cell cycle alterations and genetic instability in a human lung cell coculture model

Cited by 53 publications

References 52 publications

In Vitro and In Vivo Experimental Studies of PM2.5 on Disease Progression

In Vitro and In Vivo Experimental Studies of PM2.5 on Disease Progression

PM2.5 induces autophagy‑mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells

Fresh and ozonized black carbon promoted DNA damage and repair responses in A549 cells

Contact Info

Product

Resources

About

In vitro short-term exposure to air pollution PM2.5-0.3 induced cell cycle alterations and genetic instability in a human lung cell coculture model

Cited by 53 publications

References 52 publications

In Vitro and In Vivo Experimental Studies of PM2.5 on Disease Progression

In Vitro and In Vivo Experimental Studies of PM2.5 on Disease Progression

PM2.5&nbsp;induces autophagy‑mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells

Fresh and ozonized black carbon promoted DNA damage and repair responses in A549 cells

Contact Info

Product

Resources

About

PM2.5 induces autophagy‑mediated cell apoptosis via PI3K/AKT/mTOR signaling pathway in mice bronchial epithelium cells