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Conference Paper: Effect of fine particulate matter (PM2.5) collected in Hong Kong on mitochondrial permeability transition pore in human airway epithelial cells

TitleEffect of fine particulate matter (PM2.5) collected in Hong Kong on mitochondrial permeability transition pore in human airway epithelial cells
Authors
Issue Date2021
PublisherHong Kong Academy of Medicine Press: Open Access Journals. The Journal's web site is located at http://www.hkmj.org/
Citation
26th Medical Research Conference, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, 16 January 2021. In Hong Kong Medical Journal, 2021, v. 27 n. 1, Suppl. 1, p. 52, abstract no. 90 How to Cite?
AbstractBackground: Air pollution has been considered as the most significant environmental risk factor to human health. Fine particulate matter with aerodynamic diameter <2.5 µm (PM2.5) can penetrate into the lung reaching the large and small airways and even alveoli, causing adverse effect on the respiratory system. Our previous findings demonstrated the mitochondrial toxicity induced by PM2.5 exposure in airway cells. Recently, strong evidence is emerging that mitochondrial permeability transition pore (mPTP) may be important in certain physiological conditions and in the processes of cell damage and death. Thus, we aimed to study the effect of PM2.5 on mPTP in BEAS-2B cells. Methods: Atmospheric PM2.5 samples were collected by 47-mm Teflon filters using Desert Research Institute portable mid-volume samplers in the road site of Hong Kong. Human bronchial epithelial cell line BEAS-2B cells were cultured until 80% confluent. After arrest, cells were treated with different concentrations of PM2.5 samples to examine the ultracellular structure, intracellular calcium content, protein expressions of mPTP and apoptosis. Results: PM2.5 exposure caused mitochondrial swelling and structural damage on cristae from TEM images. In parallel, PM2.5 treatment significantly increased intracellular calcium content in a dose-dependent manner, which was accompanied by the upregulation of the major mPTP component voltage-dependent calcium channel (VDAC) expression as well as cell apoptosis. Conclusion: The current data suggest that exposure to PM2.5 collected in Hong Kong may cause mitochondriamediated apoptosis via promoting mPTP opening.
Persistent Identifierhttp://hdl.handle.net/10722/306104
ISSN
2023 Impact Factor: 3.1
2023 SCImago Journal Rankings: 0.261

 

DC FieldValueLanguage
dc.contributor.authorLiang, Y-
dc.contributor.authorChu, PH-
dc.contributor.authorTian, L-
dc.contributor.authorHo, KF-
dc.contributor.authorIp, MSM-
dc.contributor.authorMak, JCW-
dc.date.accessioned2021-10-20T10:18:50Z-
dc.date.available2021-10-20T10:18:50Z-
dc.date.issued2021-
dc.identifier.citation26th Medical Research Conference, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, 16 January 2021. In Hong Kong Medical Journal, 2021, v. 27 n. 1, Suppl. 1, p. 52, abstract no. 90-
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/306104-
dc.description.abstractBackground: Air pollution has been considered as the most significant environmental risk factor to human health. Fine particulate matter with aerodynamic diameter <2.5 µm (PM2.5) can penetrate into the lung reaching the large and small airways and even alveoli, causing adverse effect on the respiratory system. Our previous findings demonstrated the mitochondrial toxicity induced by PM2.5 exposure in airway cells. Recently, strong evidence is emerging that mitochondrial permeability transition pore (mPTP) may be important in certain physiological conditions and in the processes of cell damage and death. Thus, we aimed to study the effect of PM2.5 on mPTP in BEAS-2B cells. Methods: Atmospheric PM2.5 samples were collected by 47-mm Teflon filters using Desert Research Institute portable mid-volume samplers in the road site of Hong Kong. Human bronchial epithelial cell line BEAS-2B cells were cultured until 80% confluent. After arrest, cells were treated with different concentrations of PM2.5 samples to examine the ultracellular structure, intracellular calcium content, protein expressions of mPTP and apoptosis. Results: PM2.5 exposure caused mitochondrial swelling and structural damage on cristae from TEM images. In parallel, PM2.5 treatment significantly increased intracellular calcium content in a dose-dependent manner, which was accompanied by the upregulation of the major mPTP component voltage-dependent calcium channel (VDAC) expression as well as cell apoptosis. Conclusion: The current data suggest that exposure to PM2.5 collected in Hong Kong may cause mitochondriamediated apoptosis via promoting mPTP opening.-
dc.languageeng-
dc.publisherHong Kong Academy of Medicine Press: Open Access Journals. The Journal's web site is located at http://www.hkmj.org/-
dc.relation.ispartofHong Kong Medical Journal-
dc.relation.ispartof26th Medical Research Conference-
dc.titleEffect of fine particulate matter (PM2.5) collected in Hong Kong on mitochondrial permeability transition pore in human airway epithelial cells-
dc.typeConference_Paper-
dc.identifier.emailLiang, Y: winniell@hku.hk-
dc.identifier.emailChu, PH: phchu731@HKUCC-COM.hku.hk-
dc.identifier.emailTian, L: linweit@hku.hk-
dc.identifier.emailIp, MSM: msmip@hku.hk-
dc.identifier.emailMak, JCW: judithmak@hku.hk-
dc.identifier.authorityTian, L=rp01991-
dc.identifier.authorityIp, MSM=rp00347-
dc.identifier.authorityMak, JCW=rp00352-
dc.description.natureabstract-
dc.identifier.hkuros326837-
dc.identifier.volume27-
dc.identifier.issue1, Suppl. 1-
dc.identifier.spage52, abstract no. 90-
dc.identifier.epage52, abstract no. 90-
dc.publisher.placeHong Kong-

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