Comparative studies on regional variations in PM2.5 in the induction of myocardial hypertrophy in mice.

Abstract

Exposure to fine particulate matter (PM2.5) has been indicated to be related to an increased risk of cardiovascular diseases (CVDs) in sensitive people. However, the underlying mechanisms of PM2.5-induced CVDs are poorly understood. In the present study, PM2.5 samples were collected during winter from four cities (Taiyuan, Beijing, Hangzhou, and Guangzhou) in China. Ten-month-old C57BL/6 female mice were exposed to PM2.5 suspension at a dosage of 3\xa0mg·kg-1 (b. w.) every other day for 4\xa0weeks by oropharyngeal aspiration. PM2.5 from Taiyuan increased the blood pressure and the thicknesses of the left ventricular anterior and posterior walls, decreased the ratio of nucleus to cytoplasm in cardiomyocytes and reduced the systolic function of the heart in mice. Further investigation revealed that PM2.5 from Taiyuan induced lung inflammatory cytokines with up-regulated expressions of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). The mRNA expression levels of myocardial hypertrophy markers atrial natriuretic peptide and the β isoform of myosin heavy chain (ANP and β-MHC), matrix metalloproteinase 2 (MMP2), MMP9, and inflammatory cytokines TNF-α and IL-6 in the myocardium were significantly increased after exposure to PM2.5 of Taiyuan. Furthermore, PM2.5 from Taiyuan activated the IL-6/JAK2/STAT3/β-MHC signaling pathway in the myocardium. The correlation between the PM2.5 components and myocardial hypertrophy markers suggested that Zinc (Zn) and acenaphthene (AC) are related to the changes in ANP and β-MHC at the transcriptional level, respectively. The above results indicated that PM2.5 exposure induced myocardial hypertrophy in older mice, which might be related to the critical contributions of Zn and AC in PM2.5. The present study provides new insights into the mechanism of myocardial hypertrophy after PM2.5 exposure.