Analysis of key proinflammatory mechanisms in cardiovascular pathology through stimulation with lipopolysaccharide and urban particulate matter in mouse atrial cardiomyocytes.

Air pollution has emerged as one of the leading causes of mortality, aggravating cardiovascular diseases. Urban-particulate matter (PM) can accumulate in the cardiovascular system and through inflammation, trigger systemic damage. One of the key mechanisms of this process could be related to the activation of the inflammasome through the pre-existence of a low-grade endotoxemia and PM presence in the cells. Herein, we studied the deleterious effects of urban-PM and Lipopolysaccharide (LPS) exposure in a HL-1 mouse cardiomyocyte cell line. Urban-PM induced biological changes, including mRNA expression of pro-inflammatory genes, intracellular reactive oxygen species (ROS) generation and overexpression of inflammasome-related and structural proteins. The results revealed that urban-PM with different ultrastructure, as determined by transmission electron microscopy (TEM), is embedded inside the cardiomyocytes, leading to the recognition and activation of the inflammatory process. The increase of ROS levels and mRNA levels of pro-inflammatory genes were similarly observed in a dose-dependent manner. In addition, components and proteins of the inflammasome such as associated speck-like protein containing a CARD (ASC), caspase-1 and IL-1β were differentially overexpressed in treated HL-1 cells, as well as structural proteins like Connexin 43 (Cx43). These results provide new insights into the mechanisms that mediate innate pro-inflammatory activation in cardiomyocytes in response to air suspension pollutants.