Exosome-shuttled PCBP1 from hypoxic preconditioned urine-derived stem cells accelerates wound healing.
- 1Department of Surgery of Spine and Spinal Cord, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, No.7 Weiwu Road, Zhengzhou, 450003, Henan, China. [email protected].
- 2Department of Obstetrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, Henan, China.
- 3Department of Surgery of Spine and Spinal Cord, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, No.7 Weiwu Road, Zhengzhou, 450003, Henan, China.
Abstract
Background
We previously found that hypoxia-preconditioned human urine-derived stem cells (USCs) accelerated wound healing. Since exosomes are one of the key mediator of USCs to support skin repair, we wonder whether the healing-promoting effects of hypoxia-treated USCs were associated with exosomes.Methods
A full-thickness cutaneous wound model of female C57BL/6J mice was established. Label-free exosome proteomics was performed to investigate the differentially expression protein from exosomes derived from hypoxia-treated USCs (H-USCs-exo). Transcriptomics was carried out to explore the downstream signaling of exosome recipient cells.Results
H-USCs-exo facilitated the wound healing via angiogenesis and re-epithelialization. Also, the pro-angiogenesis results were obtained in vitro, as evidenced by the enhancement of proliferation, migration, and angiogenic abilities of human microvascular endothelial cell line HMEC-1. Subsequently, using Label-free exosome proteomics, a protein named poly (RC) binding protein 1 (PCBP1, an RNA-binding protein) was found to be significantly upregulated (Fold change = 3.34, p < 0.05) in H-USCs-exo. Exosomes delivered PCBP1 into endothelial cells, and exosomal PCBP1 mediated the pro-angiogenic effects of H-USCs-exo on HMEC-1 cells. The healing-delaying function was confirmed in mice treated with exosomes secreted by hypoxia-pretreated USCs with PCBP1 knockdown. In addition, as a tissue repair facilitator, hypoxia inducible factor 1 subunit alpha (HIF-1α) was upregulated in USCs under hypoxia condition. HIF-1α potentiated the transcription of PCBP1, leading to the high abundance of PCBP1 in H-USCs and H-USCs-exo. Further high-throughput transcriptomics illustrated that PCBP1 upregulated the expression of WNT5A (Fold change = 2.75, p < 0.05) and its downstream factors including vascular endothelial growth factor A and TEK receptor tyrosine kinase (Fold change = 2.85 and 5.75, respectively; p < 0.05).Conclusion
Exosome-shuttled PCBP1 from hypoxic preconditioned USCs accelerated wound healing, which might be associated with WNT5A signaling pathway.
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BibTeX
@article{zhang2026exosomeshuttled,
title = {{Exosome-shuttled PCBP1 from hypoxic preconditioned urine-derived stem cells accelerates wound healing.}},
author = {Xiuru Zhang and Shuangyi Zhao and Yanzheng Gao and Kun Gao and Jia Shao and Kezheng Mao and Zhongzheng Gu},
journal = {Stem cell research \& therapy},
year = {2026},
month = aug,
doi = {10.1186/s13287-026-05220-0},
url = {https://europepmc.org/article/MED/42972579},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Exosome-shuttled PCBP1 from hypoxic preconditioned urine-derived stem cells accelerates wound healing.
AU - Xiuru Zhang
AU - Shuangyi Zhao
AU - Yanzheng Gao
AU - Kun Gao
AU - Jia Shao
AU - Kezheng Mao
AU - Zhongzheng Gu
PY - 2026
DA - 2026/08/06
JO - Stem cell research & therapy
DO - 10.1186/s13287-026-05220-0
UR - https://europepmc.org/article/MED/42972579
AB - Background We previously found that hypoxia-preconditioned human urine-derived stem cells (USCs) accelerated wound healing. Since exosomes are one of the key mediator of USCs to support skin repair, we wonder whether the healing-promoting effects of hypoxia-treated USCs were associated with exosomes.Methods A full-thickness cutaneous wound model of female C57BL/6J mice was established. Label-free exosome proteomics was performed to investigate the differentially expression protein from exosomes derived from hypoxia-treated USCs (H-USCs-exo). Transcriptomics was carried out to explore the downstream signaling of exosome recipient cells.Results H-USCs-exo facilitated the wound healing via angiogenesis and re-epithelialization. Also, the pro-angiogenesis results were obtained in vitro, as evidenced by the enhancement of proliferation, migration, and angiogenic abilities of human microvascular endothelial cell line HMEC-1. Subsequently, using Label-free exosome proteomics, a protein named poly (RC) binding protein 1 (PCBP1, an RNA-binding protein) was found to be significantly upregulated (Fold change = 3.34, p < 0.05) in H-USCs-exo. Exosomes delivered PCBP1 into endothelial cells, and exosomal PCBP1 mediated the pro-angiogenic effects of H-USCs-exo on HMEC-1 cells. The healing-delaying function was confirmed in mice treated with exosomes secreted by hypoxia-pretreated USCs with PCBP1 knockdown. In addition, as a tissue repair facilitator, hypoxia inducible factor 1 subunit alpha (HIF-1α) was upregulated in USCs under hypoxia condition. HIF-1α potentiated the transcription of PCBP1, leading to the high abundance of PCBP1 in H-USCs and H-USCs-exo. Further high-throughput transcriptomics illustrated that PCBP1 upregulated the expression of WNT5A (Fold change = 2.75, p < 0.05) and its downstream factors including vascular endothelial growth factor A and TEK receptor tyrosine kinase (Fold change = 2.85 and 5.75, respectively; p < 0.05).Conclusion Exosome-shuttled PCBP1 from hypoxic preconditioned USCs accelerated wound healing, which might be associated with WNT5A signaling pathway.
SN - 1757-6512
ER -