Project description:Transcriptional profiling of the waterflea Daphnia magna, when exposed to microplastic particles made of polyvinylchloride (PVC) and the incorporated plasticizer diisononyl phtalate (DINP)
Project description:Microplastic particles that occur in the environment are coated with different biomolecules forming an eco-corona on the particles' surface, which could consequently lead to a specific interaction of the constituents of the eco-corona with membrane receptors. To date, it is not fully understood how strong microplastic particles with and without an eco-corona bind to cellular membranes and which underlying mechanisms are responsible for cellular internalization. Here we analyzed the protein composition of two different eco-coronas (freshwater and saltwater) by LC-MS/MS.
Project description:Microplastics are increasingly detected in the atmosphere and human tissues, yet their long-term effects on lung biology remain unclear. Here, we identified multiple microplastic polymers in human lung tissues using pyrolysis–gas chromatography/mass spectrometry (Py-GC/MS). Using a chronic inhalation model with environmentally relevant concentrations, we show that microplastic exposure induces progressive pulmonary fibrosis in a particle size–dependent manner, with nanoscale particles producing stronger fibrogenic effects than micron-scale particles. Single-cell transcriptomics revealed expansion of Fabp5⁺ interstitial macrophages and early fibroblast activation specifically following nanoscale exposure. Cell–cell communication analysis identified PDGFA–PDGFRA signaling as a key mediator of macrophage–fibroblast interactions. Mechanistically, nanoscale microplastics activated a Fabp5–FOXK2–PDGFA transcriptional axis in macrophages, whereas micron-scale particles showed minimal activation. Fabp5 silencing suppressed this pathway and attenuated pulmonary fibrosis, revealing a macrophage-driven mechanism linking inhaled microplastics to fibrotic lung remodeling.