In recent years, airborne fine particulate matter (PM) is drawing more public attention due to its various physicochemical features and causing pathological harm, as proven by epidemiological and clinical studies. However, the mechanism of PM-exposure-induced lung injury has not been fully characterized. Here, we established a PM-induced rat injury model for both short-term and long-term exposures at different concentrations. We employed the Fast-seq technique to profile 6316 proteins and the catTFRE approach to profile 387 transcription factors (TFs) in the lung tissue. In short-term exposure, we elucidated gradually upregulated proteins enriched in response to oxidative stress, phagosome, and the extracellula... More
In recent years, airborne fine particulate matter (PM) is drawing more public attention due to its various physicochemical features and causing pathological harm, as proven by epidemiological and clinical studies. However, the mechanism of PM-exposure-induced lung injury has not been fully characterized. Here, we established a PM-induced rat injury model for both short-term and long-term exposures at different concentrations. We employed the Fast-seq technique to profile 6316 proteins and the catTFRE approach to profile 387 transcription factors (TFs) in the lung tissue. In short-term exposure, we elucidated gradually upregulated proteins enriched in response to oxidative stress, phagosome, and the extracellular matrix (ECM)-receptor interaction pathway. Long-term exposure mainly showed the immune response pathway to be consisting of increased lymphocytes and cytokines. Intriguingly, we found that immune-related proteins were recoverable during short-term exposure. During the process of PM exposure, upregulated proteins presented dose-dependence in the lung, including stress response at low dose, minor immune response at middle dose, and severe inflammatory response at high dose. This data set provides a rich resource to facilitate the understanding of PM-induced lung damage and repair mechanism.
