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

Abstract

Background

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.

Methods

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.

Results

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.

Conclusion

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

Impact

  • 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.

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Fig. 1: Cord blood-derived platelet injection did not alter platelet parameters in neonatal rats.
Fig. 2: Cord blood derived platelets rescued arrested lung development in neonatal rats exposed to hyperoxia.
Fig. 3: Cord blood-derived platelets reduced medial wall thickening in hyperoxia-exposed neonatal rats.
Fig. 4: Hyperoxia impaired migration of primary lung fibroblasts in neonatal mice.
Fig. 5: Cord blood-derived platelets lysate restored the migration ability in myofibroblasts cultured in hyperoxia.

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Data availability

The data used to support the findings of this study are available from the corresponding author upon request.

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Acknowledgements

The authors gratefully acknowledge Dr. Lin Yi for her assistance in acquiring the umbilical cord blood.

Funding

This study is supported by National Natural Science Foundation of China (82101803 to X.C. and 82371707 to C.Y.), Guangdong Basic and Applied Basic Research Foundation (2020B1515120034 to C.Y.), Sanming Project of Medicine in Shenzhen (SZSM202211001), and Shenzhen Key Laboratory of Maternal and Child Health and Diseases (ZDSYS20230626091559006).

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Authors

Contributions

C.Y., Z.H., (Zhifeng Huang) and X.C. conceptualized and designed the study. X.C. and B.L. wrote the first draft of the manuscript. Z.H. (Zilu Huang), X.W., D.H., and L.Y. carried out the experiments. X.C. and B.L. performed the data analysis. B.L., X.C., Z.H. (Zhifeng Huang) and C.Y. reviewed and revised the manuscript. All authors read and approved the final manuscript.

Corresponding authors

Correspondence to Zhifeng Huang or Chuanzhong Yang.

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Chen, X., Lin, B., Huang, Z. et al. Umbilical cord blood platelet lysate preserves myofibroblast migration and mitigates hyperoxic lung injury. Pediatr Res (2025). https://doi.org/10.1038/s41390-025-04422-1

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