Ambient fine particles (PM<sub>2.5</sub>) attenuate collagen‐induced platelet activation through interference of the PLCγ2/Akt/GSK3β signaling pathway

Yin, Zhang; Xu, Hui; Yao, Xiali; Li, Gang; Nie, Chunjie; Han, Wei; Cai, Li; Liang, Minglu; Ming, Zhang-Yin; Zhang, Xiaojian

doi:10.1002/tox.22257

Cited by 6 publications

(1 citation statement)

References 45 publications

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“…Scanning electron microscopy was digitized and particle area measurements were made. The equivalent spherical diameter (ESD), a commonly used parameter for particle sizing, was calculated using the formula: ESD = 2 × (area / π) 1/2 [18].…”

Section: Methodsmentioning

confidence: 99%

Metabolomics analysis reveals that benzo[a]pyrene, a component of PM2.5, promotes pulmonary injury by modifying lipid metabolism in a phospholipase A2-dependent manner in vivo and in vitro

et al. 2017

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Particulate matter with an aerodynamic diameter less than 2.5 μM (PM2.5) is one of the major environmental pollutants in China. In this study, we carried out a metabolomics profile study on PM2.5-induced inflammation. PM2.5 from Beijing, China, was collected and given to rats through intra-tracheal instillation in vivo. Acute pulmonary injury were observed by pulmonary function assessment and H.E. staining. The lipid metabolic profile was also altered with increased phospholipid and sphingolipid metabolites in broncho-alveolar lavage fluid (BALF) after PM2.5 instillation. Organic component analysis revealed that benzo[a]pyrene (BaP) is one of the most abundant and toxic components in the PM2.5 collected on the fiber filter. In vitro, BaP was used to treat A549 cells, an alveolar type II cell line. BaP (4 μM, 24 h) induced inflammation in the cells. Metabolomics analysis revealed that BaP (4 μM, 6 h) treatment altered the cellular lipid metabolic profile with increased phospholipid metabolites and reduced sphingolipid metabolites and free fatty acids (FFAs). The proportion of ω–3 polyunsaturated fatty acid (PUFA) was also decreased. Mechanically, BaP (4 μM) increased the phospholipase A2 (PLA2) activity at 4 h as well as the mRNA level of Pla2g2a at 12 h. The pro-inflammatory effect of BaP was reversed by the cytosolic PLA2 (cPLA2) inhibitor and chelator of intracellular Ca2+. This study revealed that BaP, as a component of PM2.5, induces pulmonary injury by activating PLA2 and elevating lysophosphatidylcholine (LPC) in a Ca2+-dependent manner in the alveolar type II cells.

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Section: Methodsmentioning

confidence: 99%

Metabolomics analysis reveals that benzo[a]pyrene, a component of PM2.5, promotes pulmonary injury by modifying lipid metabolism in a phospholipase A2-dependent manner in vivo and in vitro

et al. 2017

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Impacts of Air Pollution on Epidemiology and Cardiovascular Systems

Prasad

Paudel

2020

Environmental Chemistry for a Sustainable World

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Association of polycyclic aromatic hydrocarbons exposure with atherosclerotic cardiovascular disease risk: A role of mean platelet volume or club cell secretory protein

Hou

Zhou

et al. 2018

Environmental Pollution

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Ambient fine particles (PM_2.5) attenuate collagen‐induced platelet activation through interference of the PLCγ2/Akt/GSK3β signaling pathway

Abstract: PM attenuated collagen-induced platelet aggregation, α-granule secretion and adhesion, with the potential mechanism of impairing PLCγ2, Akt, and GSK3β signaling. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 530-540, 2017.

Cited by 6 publications

References 45 publications

Metabolomics analysis reveals that benzo[a]pyrene, a component of PM2.5, promotes pulmonary injury by modifying lipid metabolism in a phospholipase A2-dependent manner in vivo and in vitro

Metabolomics analysis reveals that benzo[a]pyrene, a component of PM2.5, promotes pulmonary injury by modifying lipid metabolism in a phospholipase A2-dependent manner in vivo and in vitro

Impacts of Air Pollution on Epidemiology and Cardiovascular Systems

Association of polycyclic aromatic hydrocarbons exposure with atherosclerotic cardiovascular disease risk: A role of mean platelet volume or club cell secretory protein

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Ambient fine particles (PM2.5) attenuate collagen‐induced platelet activation through interference of the PLCγ2/Akt/GSK3β signaling pathway

Abstract: PM attenuated collagen-induced platelet aggregation, α-granule secretion and adhesion, with the potential mechanism of impairing PLCγ2, Akt, and GSK3β signaling. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 530-540, 2017.

Cited by 6 publications

References 45 publications

Metabolomics analysis reveals that benzo[a]pyrene, a component of PM2.5, promotes pulmonary injury by modifying lipid metabolism in a phospholipase A2-dependent manner in vivo and in vitro

Metabolomics analysis reveals that benzo[a]pyrene, a component of PM2.5, promotes pulmonary injury by modifying lipid metabolism in a phospholipase A2-dependent manner in vivo and in vitro

Impacts of Air Pollution on Epidemiology and Cardiovascular Systems

Association of polycyclic aromatic hydrocarbons exposure with atherosclerotic cardiovascular disease risk: A role of mean platelet volume or club cell secretory protein

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Ambient fine particles (PM_2.5) attenuate collagen‐induced platelet activation through interference of the PLCγ2/Akt/GSK3β signaling pathway