Exposure to real-ambient particulate matter induced vascular hypertrophy through activation of PDGFR beta

Background: Vascular toxicity induced by particulate matter (PM) exposure exacerbates the onset and develop-ment of cardiovascular diseases; however, its detailed mechanism remains unclear. Platelet-derived growth factor receptor beta (PDGFR beta) acts as a mitogen for vascular smooth muscle cells (VSMCs) and is therefore essential for normal vasoformation. However, the potential effects of PDGFR beta on VSMCs in PM-induced vascular toxicity have not yet been elucidated.Methods: To reveal the potential roles of PDGFR beta signalling in vascular toxicity, individually ventilated cage (IVC)-based real-ambient PM exposure system mouse models and PDGFR beta overexpression mouse models were established in vivo, along with in vitro VSMCs models.Results: Vascular hypertrophy was observed following PM-induced PDGFR beta activation in C57/B6 mice, and the regulation of hypertrophy-related genes led to vascular wall thickening. Enhanced PDGFR beta expression in VSMCs aggravated PM-induced smooth muscle hypertrophy, which was attenuated by inhibiting the PDGFR beta and janus kinase 2 /signal transducer and activator of transcription 3 (JAK2/STAT3) pathways.Conclusion: Our study identified the PDGFR beta gene as a potential biomarker of PM-induced vascular toxicity. PDGFR beta induced hypertrophic effects through the activation of the JAK2/STAT3 pathway, which may be a biological target for the vascular toxic effects caused by PM exposure.