WANG Hui-min, CHEN Tao, TONG Jian, JIANG Yan. Disruption of cardiac differentiation by PM2.5 in vitro[J]. Journal of Environmental and Occupational Medicine, 2018, 35(6): 536-540. DOI: 10.13213/j.cnki.jeom.2018.17744
Citation: WANG Hui-min, CHEN Tao, TONG Jian, JIANG Yan. Disruption of cardiac differentiation by PM2.5 in vitro[J]. Journal of Environmental and Occupational Medicine, 2018, 35(6): 536-540. DOI: 10.13213/j.cnki.jeom.2018.17744

Disruption of cardiac differentiation by PM2.5 in vitro

  • Objective To study the effect of PM2.5 exposure on cardiac differentiation.

    Methods P19 mouse carcinoma stem cells were used as an in vitro cardiac differentiation model, and MTT assay was performed to examine the cytoplasmic toxicity of PM2.5 exposure at different concentrations (0, 1, 10, and 100 mg/L). The cells were exposed to PM2.5 at the non-cytotoxic concentration of 10 mg/L for 48 h before the differention was initiated. After the differentiation was initiated, the morphological changes were observed, the expression changes of cardiac specific genes (OCT4, pluripotent gene; ISL-1, precursor formation related gene; MLC2V, highly expressed at maturation period) were evaluated by real-time fluorescence quantitative PCR, and the expression efficiency of cardiac functional protein cardiac troponin T (cTNT) by immunofluorescence and flow cytometry.

    Results Compared with the control group, the PM2.5 groups showed cell morphological changes and the cardiac specific genes were abnormally expressed across all differentiation stages. OCT4 expression was reduced by 80% before differentiation (P < 0.01), and increased after differentiation (P < 0.05); ISL-1 expression was reduced to 59% of the control group in precursor formation period (P < 0.01); MLC2V expression was reduced to 39% of the control group in maturation period (P < 0.01). Besides, the cardiac functional protein cTNT decreased its expression from 61% to 47% after PM2.5 exposure, but there was no difference.

    Conclusion Early exposure to PM2.5 during the cardiac development may disturb cardiac differentiation of stem cells.

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