Figure 8
Hypothetic model for the mechanism of the antiapoptotic effect of PM 2.5 . Exposure of bronchial epithelial cells to PM2.5, leads to particles endocytosis and PAH desorption. Then, intracellular PAH can target and activate the aryl hydrocarbon receptor (AhR). It is noteworthy, that AhR translocates to the nucleus to bind to specific xenobiotic responsive elements (XRE) in the promoter of its target genes; some of them might be mitochondrial MMP regulators (dotted arrow), thus might protect the cell from apoptosis induced by A23187, staurosporin (STS) or oligomycin (Omy). Moreover, the water-soluble compounds of PM2.5 also have antiapoptotic activity, but the pathway involved is still under investigation (dotted arrow). Illustration carried out thanks to Servier Medical Art.