June 2020
Volume 61, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2020
NEDD4-mediated Protein Ubiquitination Enhances Corneal Epithelial Wound Healing
Author Affiliations & Notes
  • Dongsheng Yan
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, China
  • Xuemei Ling
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, China
  • Jingjing Tang
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, China
  • Peter S. Reinach
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, China
  • Footnotes
    Commercial Relationships   Dongsheng Yan, None; Xuemei Ling, None; Jingjing Tang, None; Peter S. Reinach, None
  • Footnotes
    Support  973 Project (2012CB722303) from the Ministry of Science and Technology of China, and Science Foundation of Wenzhou Medical University (QTJ11020).
Investigative Ophthalmology & Visual Science June 2020, Vol.61, 161. doi:
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    • Get Citation

      Dongsheng Yan, Xuemei Ling, Jingjing Tang, Peter S. Reinach; NEDD4-mediated Protein Ubiquitination Enhances Corneal Epithelial Wound Healing. Invest. Ophthalmol. Vis. Sci. 2020;61(7):161.

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

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Abstract

Purpose : Neural precursor cell-expressed developmentally down-regulated protein 4 (NEDD4) is an important E3 ubiquitin ligase which is implicated in multiple biological processes. However, its role in regulating corneal epithelial renewal, remains elusive. In the present study, we investigated the functional role that NEDD4 may play in corneal epithelial wound healing (CEWH) process.

Methods : Western blotting was performed to detect Nedd4 expression during mouse CEWH. Specific siRNA targeting NEDD4 was transfected into human corneal epithelial cells (HCECs) using Lipofectamine RNAiMAX reagent. MTS, Flow cytometry, and wound-healing assay evaluated the effects of NEDD4 knockdown on cell proliferation, cell cycle progression, and migration, respectively. The effects of NEDD4 knockdown on in vivo wound healing were evaluated using a murine corneal epithelial debridement model by monitoring corneal fluorescein staining.

Results : Nedd4 expression level was significantly upregulated during mouse CEWH. Knockdown of NEDD4 significantly inhibited HCEC proliferation by inducing cell cycle G2 arrest and suppressed cell migration. Furthermore, Nedd4 knockdown remarkably retarded in vivo CEWH. In addition, downregulation of NEDD4 decreased p-Akt level in HCECs.

Conclusions : Our results demonstrate that NEDD4-mediated ubiquitination contributes to promoting CEWH through activation of the Akt signaling pathway.

This is a 2020 ARVO Annual Meeting abstract.

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