Fig. 6.

Schematic representation of hypothesis. Hyperoxia exposure decreases VASP expression and phosphorylation disrupting actin dynamics in human tissues. Early responses include increases in cofilin1 in attempts to initiate repair. In later stages of injury and dysregulated repair, we observe decreases in VASP phosphorylation and profilin1 which are indicative of impaired repair. L-MSCs play a significant role in repair and proliferate in response to injury stimuli. Early increase in CD146 is indicative of enhanced L-MSCs proliferation and homing in mouse lungs, while at later stages decreased CD146 in human autopsy tissue is suggestive injury beyond repair. We speculated that disruptions in ABP dynamics may be due to interventions or morbidities other than hyperoxia alone in humans with BPD