Adverse impact of ambient PM2.5 on expression and trafficking of surfactant protein A through reactive oxygen species damage to lamellar bodies

Peng, Juanjuan; Zhang, Lingli; Meng, Qingqi; Zhang, Feng; Mao, Xiaoning; Liu, Juman; Chen, Yinhui; Zou, Huafang; Shi, Bao; Wu, Ruijian; Huang, Binglong; Huang, Yuge; Tan, Jianxin; Feng, Cheng; Zhang, Xingliang

doi:10.1016/j.toxlet.2019.08.015

Cited by 9 publications

(6 citation statements)

References 28 publications

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“…The phospholipid film of dipalmitoyl phosphatidylcholine on the surface of lung alveoli reduces surface tension for optimal gas exchange and builds a hydrophobic protective lining as environmental barrier ( Schmitz and Müller, 1991 ; Menon et al, 2018 ). One study indicated that lamellar bodies in A549 cells disappear compared with the control when exposed to 100μgPM 2.5 ( Peng et al, 2019 ). A similar change was also observed in our studies.…”

Section: Discussionmentioning

confidence: 99%

Amelioration of Ambient Particulate Matter (PM2.5)-Induced Lung Injury in Rats by Aerobic Exercise Training

Qin

Fan

et al. 2021

Front. Physiol.

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Ambient particulate matter (PM2.5), as an inflammation-inducing factor, increases the prevalence of lung injury. The aim of this study was to examine the protective effect and mechanism of aerobic exercise on PM2.5 exposure-induced lung injury. Forty Wistar rats were randomly divided into four groups: sedentary+PM2.5 exposure, exercise+PM2.5 exposure, sedentary, and exercise groups. All rats in the exercise-related groups underwent 8-week aerobic interval treadmill training (5daysweek−1, 1hday−1). PM-exposed rats were exposed to ambient PM2.5 (6h day−1) for 3weeks after the 8-week exercise intervention. Then, ventilation function, histopathological changes, and inflammation responses of pulmonary tissue were examined. Results showed that PM2.5 exposure induced lung injury as manifested by decreased pulmonary function, abnormal histopathological changes, and increased pro-inflammatory cytokine levels (tumor necrosis factor-α and Interleukin-1α). Aerobic exercise alleviated the airway obstruction, reduced respiratory muscle strength, bronchial mucosal exfoliation, ultrastructure damage, and inflammatory responses induced by PM2.5 in exercise-related groups. The benefits of exercise were related with the downregulation of p38-mitogen-activated protein kinase (MAPK), and the subsequent inhibition of the pathways of the cyclooxygenase 2 (COX-2) product, prostaglandin E2 (PGE2). Thus, pre-exercise training may be an effective way to protect against PM2.5-induced lung inflammatory injury in rats.

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Section: Discussionmentioning

confidence: 99%

Amelioration of Ambient Particulate Matter (PM2.5)-Induced Lung Injury in Rats by Aerobic Exercise Training

Qin

Fan

et al. 2021

Front. Physiol.

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“…Based on our published method [8, 10, 11], the left lung sections were stained with hematoxylin and eosin (C0105; Beyotime, Shanghai, China) and periodic acid-Schiff (PAS) (G1280; Solarbio, Beijing, China). Based on the published method [10, 12], the blinded histopathological score was used to assess the degree of peribronchial and alveolar structural changes on a subjective scale of 0–3: 0, airway epithelial cells remain intact; 1, lung parenchyma becomes dense, alveolar cavity becomes narrowed; 2, columnar cells become damaged; and 3, airway wall is destroyed with visible effusion.…”

Section: Methodsmentioning

confidence: 99%

“…The protein expression levels were detected by Western blot as described previously [11]. Total β-catenin rabbit antibody (1:2,000, #8480, Cell Signaling Technology [CST]), non-phospho (active) β-catenin rabbit antibody (1:2,000, #8814S, CST), β-actin rabbit antibody (1:3,000, #4967S, CST), and horseradish peroxidase-conjugated anti-rabbit IgG (1:2,000, #7074, CST) were used for antigen-antibody reaction.…”

Section: Methodsmentioning

confidence: 99%

Divergent Roles of miR-3162-3p in Pulmonary Inflammation in Normal and Asthmatic Mice as well as Antagonism of miR-3162-3p in Asthma Treatment

Liu

Chen

Zhang

et al. 2020

Int Arch Allergy Immunol

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MicroRNA (miRNA) mimics or antagomirs hold great promise for asthma treatment compared with glucocorticoids as mainstay therapy for asthma. But the role of miRNA in regulating asthmatic inflammation is largely unclear. We previously reported that miR-3162-3p in the peripheral blood of children with asthma was obviously upregulated compared to that in healthy children. This study aimed to elucidate the role of miR-3162-3p in pulmonary inflammation in normal and asthmatic mice as well as preliminarily explore the potential of miR-3162-3p antagomir in asthma treatment. A noninvasive whole-body plethysmograph measured airway responsiveness. Both qRT-PCR and Western blot were used to detect the expression of miRNA, mRNA, or protein. Cells in bronchoalveolar lavage fluid were counted by platelet counting and Wright's staining. Inflammatory infiltration and mucus secretion were identified by hematoxylin and eosin and periodic acid-Schiff staining, respectively. Cytokines in the lungs were detected by ELISA. The miR-3162-3p mimic intraperitoneally administered to normal mice decreased β-catenin levels in the lungs without obviously altering the lung histology and cytokine levels. Antagonizing miR-3162-3p in ovalbumin-induced asthmatic mice effec-Juman Liua, Yinhui Chena, and Feng Zhang contributed equally to this work. Edited by: H.-U. Simon, Bern.

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“…Numerous studies have reported that some trace elements (e.g., Fe, Ni, Zn, V, Pb, As, Se, Cd, and Hg) may cause damage to cells, tissues, proteins, and DNA and change cell permeability by inducing the production of reactive oxygen species (ROS) [ 175 , 176 , 177 ]. For example, an extensive increase in ROS can be caused by Fe in vivo, causing oxidative damage and inflammation [ 178 ]. Gilli et al found that oxidative DNA damage attributed to PM is also related to the Fe content [ 179 ].…”

Section: Health Effects Of Indoor Pmmentioning

confidence: 99%

Indoor Particulate Matter in Urban Households: Sources, Pathways, Characteristics, Health Effects, and Exposure Mitigation

Zhang

Magana-Arachchi

et al. 2021

IJERPH

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Particulate matter (PM) is a complex mixture of solid particles and liquid droplets suspended in the air with varying size, shape, and chemical composition which intensifies significant concern due to severe health effects. Based on the well-established human health effects of outdoor PM, health-based standards for outdoor air have been promoted (e.g., the National Ambient Air Quality Standards formulated by the U.S.). Due to the exchange of indoor and outdoor air, the chemical composition of indoor particulate matter is related to the sources and components of outdoor PM. However, PM in the indoor environment has the potential to exceed outdoor PM levels. Indoor PM includes particles of outdoor origin that drift indoors and particles that originate from indoor activities, which include cooking, fireplaces, smoking, fuel combustion for heating, human activities, and burning incense. Indoor PM can be enriched with inorganic and organic contaminants, including toxic heavy metals and carcinogenic volatile organic compounds. As a potential health hazard, indoor exposure to PM has received increased attention in recent years because people spend most of their time indoors. In addition, as the quantity, quality, and scope of the research have expanded, it is necessary to conduct a systematic review of indoor PM. This review discusses the sources, pathways, characteristics, health effects, and exposure mitigation of indoor PM. Practical solutions and steps to reduce exposure to indoor PM are also discussed.

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Adverse impact of ambient PM2.5 on expression and trafficking of surfactant protein A through reactive oxygen species damage to lamellar bodies

Cited by 9 publications

References 28 publications

Amelioration of Ambient Particulate Matter (PM2.5)-Induced Lung Injury in Rats by Aerobic Exercise Training

Amelioration of Ambient Particulate Matter (PM2.5)-Induced Lung Injury in Rats by Aerobic Exercise Training

Divergent Roles of miR-3162-3p in Pulmonary Inflammation in Normal and Asthmatic Mice as well as Antagonism of miR-3162-3p in Asthma Treatment

Indoor Particulate Matter in Urban Households: Sources, Pathways, Characteristics, Health Effects, and Exposure Mitigation

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