June 2021
Volume 62, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2021
PRMT1 Enhances Corneal Epithelial Wound Healing
Author Affiliations & Notes
  • Peter Reinach
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, Zhejiang, China
  • Qiongjie Cao
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, Zhejiang, China
  • Dongsheng Yan
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, Zhejiang, China
  • Footnotes
    Commercial Relationships   Peter Reinach, None; Qiongjie Cao, None; Dongsheng Yan, None
  • Footnotes
    Support  Science Foundation of Wenzhou Medical University QTJ11020
Investigative Ophthalmology & Visual Science June 2021, Vol.62, 845. doi:
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      Peter Reinach, Qiongjie Cao, Dongsheng Yan; PRMT1 Enhances Corneal Epithelial Wound Healing. Invest. Ophthalmol. Vis. Sci. 2021;62(8):845.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose : Post-translational protein arginine methylation is a fundamental modification of many different essential cellular processes. Protein arginine methyltransferase 1 (PRMT1) is a type I member of the PRMT family, and it is critical for catalyzing such modulation. However, its role in mediating corneal epithelial renewal remains unknown. In the present study, we characterize its involvement in corneal epithelial wound healing (CEWH) and thereby gain insight into how it affects this process.

Methods : An Alger brush was used to debride the corneal epithelium in mice. Western blot was performed to detect the PRMT1 protein expression level during CEWH in this tissue. Human corneal epithelial cells (HCECs) were transfected with siRNA targeted to knock down PRMT1 expression using Lipofectamine RNAiMAX. MTS and a scratch wound-healing assay evaluated the effects of PRMT1 on HCEC proliferation and migration, respectively. Flow cytometry determined cell cycle progression. Corneal epithelial-specific Prmt1 deletion mice were generated using the Cre-lox system.

Results : The PRMT1 protein expression level was significantly upregulated during CEWH. Prmt1 deletion significantly delayed in vivo CEWH. Furthermore, downregulation of PRMT1 only inhibited HCEC migration without altering either their cell cycle progression or proliferation.

Conclusions : PRMT1 upregulation promotes CEWH through stimulating cell migration. This association indicates that increasing the protein arginine methylation status warrants further evaluation as a potential option to promote this process in a clinical setting.

This is a 2021 ARVO Annual Meeting abstract.


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