Umbilical cord blood platelet lysate preserves myofibroblast migration and mitigates hyperoxic lung injury

Traditionally, platelets were thought to originate solely in the bone marrow, but emerging evidence now indicates that the lung is a major site of platelet generation. Our previous work, along with studies by others, has revealed decreased platelet counts and enhanced platelet activation in BPD patients, linking platelets to the disease's pathogenesis.

We investigated the protective effects and underlying mechanisms of umbilical cord blood (UCB) platelets in mitigating hyperoxia-induced lung injury in neonatal rats and in vitro.

Compared with platelet-poor plasma (PPP), UCB-derived platelets (PLT) treatment preserved lung development, as evidenced by an increased density of secondary crests and reduced small arterial wall thickness. Given that secondary crest formation depends on myofibroblast activity, we further examined the cellular function of myofibroblasts isolated from the lungs of control and hyperoxic mice. We found that hyperoxia impaired myofibroblast function, particularly their migration capacity, which can be prevented by UCB platelet lysate.

These findings suggest that UCB PLT preserve lung development by protecting myofibroblast migratory capacity, offering new insights into BPD pathogenesis and potential therapeutic strategies.

Hyperoxia impairs myofibroblast function, particularly their migratory capacity, which can be prevented by umbilical cord blood platelet lysate. Umbilical cord blood platelets preserve lung development in hyperoxia-exposed newborn rats by increasing the density of secondary crests and mitigating vascular remodeling in small arteries. These findings underscore the promising therapeutic potential of umbilical cord blood-derived platelets for the management of BPD.