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NEAT1 promotes keratinocyte migration and proliferation during wound healing by regulating miR-26a-5p/LGR4 axis

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Abstract

Background

Wound re-epithelialization is considered as an extremely important link in the complete reconstruction of the epidermal barrier. The present study is aimed to determine the association between transforming growth factor β (TGF-β) and re-epithelialization.

Objective

It was aimed to explore the possible molecular mechanism of TGF-β mediated re-epithelialization.

Results

NEAT1 was upregulated in TGF-β1-treated HaCaT cells and promoted cell proliferation. NEAT1 overexpression enhanced the wound healing and upregulated MMP-2 and MMP-9 in TGF-β1-treated HaCaT cells. Mechanically, TGF-β1 down-regulated miR-26a-5p through targeting NEAT1 in HaCaT cells. Furthermore, NEAT1/miR-26a-5p axis regulated the expression of LGR4 in HaCaT cells. Finally, the results showed that NEAT1/miR-26a-5p/LGR4 axis was involved in TGF-β1-mediated re-epithelialization.

Conclusion

NEAT1/miR-26a-5p/LGR4 network is an important participant in TGF-β1-mediated keratinocyte proliferation and migration, which provides a novel perspective for understanding the cellular behavior and related molecular events in re-epithelialization.

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Authors

Contributions

LZ, RT and KW designed the study, supervised the data collection, analyzed the data, interpreted the data, prepared the manuscript for publication and reviewed the draft of the manuscript. All authors have read and approved the manuscript.

Corresponding author

Correspondence to Kui Wang.

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Author Lan Zhang declares that he/she has no conflict of interest; author Rong Tian declares that he/she has no conflict of interest; author Kui Wang declares that he/she has no conflict of interest.

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Zhang, L., Tian, R. & Wang, K. NEAT1 promotes keratinocyte migration and proliferation during wound healing by regulating miR-26a-5p/LGR4 axis. Mol. Cell. Toxicol. 19, 473–481 (2023). https://doi.org/10.1007/s13273-022-00275-5

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