Quantitative Analysis of Piezo Receptors as Mechanosensitive Targets in Bronchopulmonary Dysplasia Recovery

Bronchopulmonary dysplasia (BPD) is a chronic lung disease affecting premature infants exposed to prolonged oxygen therapy and mechanical ventilation. Beyond pulmonary injury, BPD is increasingly recognized as a multisystem disorder involving cardiovascular remodeling. Piezo mechanosensitive ion channels regulate mechanotransduction, vascular remodeling, and inflammatory signaling, making them promising therapeutic targets. In parallel, mesenchymal stromal cell-derived extracellular vesicles (MSC-EVs) have emerged as potential regenerative therapies; however, their effects on Piezo receptor expression remain unclear. This study investigated Piezo1 and Piezo2 expression in the cardiac tissue of neonatal rats exposed to hyperoxia, an established experimental BPD model, evaluating the effects of MSC-EV treatment. Histological examination revealed preserved myocardial architecture in all experimental groups. According to immunofluorescence data, hyperoxic exposure increased the immunoreactivity of both Piezo receptors, with a statistically significant increase observed only for Piezo2. Following MSC-EV treatment, Piezo1 and Piezo2 immunoreactivity decreased compared with untreated hyperoxic animals, approaching normoxic levels, although these changes were not statistically significant. These findings provide preliminary evidence that hyperoxia alters cardiac mechanosensitive signaling and suggest that MSC-EVs may contribute to restoring myocardial mechanosensitive homeostasis, supporting further investigation of Piezo receptors as potential therapeutic targets in BPD.