Lnc-Clic5 as a sponge for miR-212-5p to inhibit cow barn PM-induced apoptosis in rat alveolar macrophages.

Particulate matter (PM) is a highly hazardous airborne particulate matter that poses a significant risk to humans and animals. Urban airborne particulate matter contributes to the increased incidence and mortality of respiratory diseases, such as asthma and chronic obstructive pulmonary disease (COPD), in humans. However, the specific mechanism by which PM affects animals in barn environments is yet to be elucidated. In this study, we investigated the effect of exposure to cow barn PM on rat alveolar macrophages (NR8383) and found that it induced apoptosis via the miR-212-5p/RASSF1 pathway. We found that lnc-Clic5 expression was downregulated in NR8383 cells exposed to cow barn PM. Lnc-Clic5 plays a competitive endogenous RNA (ceRNA) regulatory role by sponging miR-212-5p to attenuate the regulation of RASSF1. Moreover, lnc-Clic5 overexpression inhibited NR8383 apoptosis by targeting the miR-212-5p/RASSF1 pathway. Co-treatment with miR-212-5p and lnc-Clic5 in the presence of cow barn PM revealed that lnc-Clic5 reversed NR8383 cell apoptosis induced by PM when miR-212-5p was overexpressed. These findings contribute to the study of ncRNAs and ceRNAs regulating PM-induced apoptosis in animal farms, provide therapeutic targets for lung macrophage apoptosis, and may be useful for further evaluating the toxicological effects of PM in farmhouses on the respiratory systems of humans and animals.