title: [PM2.5from traffic-related ambient air and wood smoke induces epithelial-mesenchymal transition in human bronchial epithelial cells].
abstract: Objective:To observe if arterial traffic ambient PM2.5(TAPM2.5) and wood smoke PM2.5(WSPM2.5) exposure can induce epithelial-mesenchymal transition (EMT) in human bronchial cells (HBEC).Methods:PM2.5was collected from an arterial traffic road and a typical southern kitchen, and then the collections were extracted by DMSO. The viability of HBEC was measured by Cell Counting Kit (CCK-8) after culture with PM2.5-DMSO extracts for 24 hours. The expressions of EMT markers, including E-cadherin, cytokeratin, α-smooth muscle actin (α-SMA), vimentin and collagen typeⅠ (COL-Ⅰ) in HBEC were assayed by cell immunofluorescence and Western blot analysis after exposed to two different sources of PM2.5-DMSO extracts for 14 days.Results:The cell viability of HBEC increased at low concentrations (1, 2, 10 μg/ml and 1, 5, 10 μg/ml, corresponding to [(118.4±13.7)%, (118.2±8.0)%, (123.0±19.6)% and (112.4±4.1)%, (120±5.4)%, (117.8±7.0)%, respectively, allP<0.05], and then declined at high levels [20, 100, 200 μg/ml and 15, 20, 30, 40 μg/ml, corresponding to (100.7±12.1)%, (53.4±15.3)%, (9.4±1.7)% and (106.8±10.0)%, (93.8±7.9)%, (60.9±9.5)%, (46.2±3.6)%, respectively,Pvalues were 0.923, 0.000, 0.000 and 0.231, 0.278, 0.000, 0.000, respectively] in both TAPM2.5-DMSO and WSPM2.5-DMSO incubation. After exposure for 14 days, the cells lost their typical cobblestone-like shape which implied that EMT might occur. The same treatment caused decreased positive signals of E-cadherin and cytokeratin in a small proportion of the cells. The decreased expressions of cytokeratin were verified by Western blot (TAPM2.5and WSPM2.5were 0.063±0.109 and 0.039±0.313,Pvalues were 0.033 and 0.030, respectively), while α-SMA was only significantly upregulated in the WSPM2.5-DMSO group (7.853±4.784,P=0.049). The expressions of E-cadherin decreased in both groups but not statistically significant in Western blot (0.862±0.096 and 0.817±0.212,Pvalues were 0.228 and 0.117, respectively). Another marker of EMT, COL-I, markedly increased in both PM2.5treatment groups (2.549±1.037 and 3.658±1.207,Pvalues were 0.034 and 0.001).Conclusions:Both PM2.5from arterial traffic ambient air and wood smoke could induce EMT in human bronchial epithelial cells, while WSPM2.5appeared to have a more significant influence on EMT in HBEC.
authors: State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, the First Affiliated Hospital, Guangzhou Medical University, Guangzhou 510120, China.
authors: J D
authors: JD
authors: Pu
authors: L M
authors: LM
authors: Huang
authors: X Q
authors: XQ
authors: Ye
authors: W
authors: W
authors: Hong
authors: W F
authors: WF
authors: Zou
authors: J
authors: J
authors: Xu
authors: B
authors: B
authors: Li
authors: P X
authors: PX
authors: Ran
mesh_terms: D000199:Actins; D000393:Air Pollutants / Q000009:adverse effects*; D015703:Antigens, CD; D015153:Blotting, Western; D015820:Cadherins; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects*; D006801:Humans; D018986:Motor Vehicles; D052638:Particulate Matter / Q000009:adverse effects*; D012906:Smoke / Q000009:adverse effects*; D014026:Nicotiana; D014746:Vimentin; D014934:Wood
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; D000393:Air Pollutants; D015703:Antigens, CD; C513384:CDH1 protein, human; D015820:Cadherins; D052638:Particulate Matter; D012906:Smoke; D014746:Vimentin