PM2.5 exposure exacerbates mice thoracic aortic aneurysm and dissection by inducing smooth muscle cell apoptosis via the MAPK pathway.

Air pollution is a major public health concern worldwide. Exposure to fine particulate matter (PM2.5) is closely associated with cardiovascular diseases. However, the effect of PM2.5 exposure on thoracic aortic aneurysm and dissection (TAAD) has not been fully elucidated. Diesel exhaust particulate (DEP) is an important component of PM2.5, which causes health effects and is closely related to the incidence of cardiovascular disease. In the current study, we found that DEP exposure increased the incidence of aortic dissection (AD) in β-aminopropionitrile (BAPN)-induced thoracic aortic aneurysm (TAA). In addition, exposure to PM2.5 increased the diameter of the thoracic aorta in mice models. The number of apoptotic cells increased in the aortic wall of PM2.5-treated mice, as did the protein expression level of BAX/Bcl2 and cleaved caspase3/caspase3. Using a rhythmically stretching aortic mechanical simulation model, fluorescent staining indicated that PM2.5 administration could induce mitochondrial dysfunction and increase reactive oxygen species (ROS) levels in human aortic smooth muscle cells (HASMCs). Furthermore, ERK1/2 mitogen-activated protein kinase (MAPK) signaling pathways participated in the apoptosis of HASMCs after PM2.5 exposure. Therefore, we concluded that PM2.5 exposure could exacerbate the progression of TAAD, which could be induced by the increased apoptosis in HASMCs through the ERK1/2 MAPK signaling pathway.