July 2019
Volume 60, Issue 9
ARVO Annual Meeting Abstract  |   July 2019
Lidocaine blocks the proliferation, migration, and Epithelial-Mesenchymal Transition of Human Retinal Epithelial cells
Author Affiliations & Notes
  • Yoon Hyung Kwon
    Department of ophthalmology, Dong-A University Hospital, Busan, Korea (the Republic of)
  • Min Seok Woo
    Department of Convergence Medical Science, Gyeongsang National University, Jinju, Korea (the Republic of)
  • Yeon A Kim
    Department of Anesthesiology and Pain Medicine, Gyeongsang National University Changwon Hospital, Changwon, Korea (the Republic of)
  • Footnotes
    Commercial Relationships   Yoon Hyung Kwon, None; Min Seok Woo, None; Yeon A Kim, None
  • Footnotes
    Support   National Research Foundation of Korea (NRF) grant funded by the Korean Government (NRF-2017R1C1B5017925).
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 5807. doi:https://doi.org/
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      Yoon Hyung Kwon, Min Seok Woo, Yeon A Kim; Lidocaine blocks the proliferation, migration, and Epithelial-Mesenchymal Transition of Human Retinal Epithelial cells. Invest. Ophthalmol. Vis. Sci. 2019;60(9):5807. doi: https://doi.org/.

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

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Purpose : Proliferative vitroretinopathy (PVR) is a major cause of failure in surgery of rhegmatogenous retinal detachment (RRD). The strategy for precautions or resolving the PVR is very limited. Lidocaine is well known and widely used local anesthetics. We evaluated the effects of lidocaine on epithelial-mesenchymal transition (EMT) and migration in retinal pigment epithelial cells, which is major cell type involved in the development of PVR, and its mechanism.

Methods : Adult retinal pigmented epithelial 19 (ARPE 19) cell line was used and MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) assay was performed with various concentrations of lidocaine. We induced ARPE to EMT by TGF-β1 and it was demonstrated with western blot of α-SMA (smooth muscle actin), vimentin, E-cadherin, and collagen I. The inhibitory effects of lidocaine in TGF-β1 signaling were also evaluated with western blot of ERK (extracellular signal regulated kinase), PI3K (Phosphoinositide 3-kinase), Akt (Protein kinase B), and smad. The change of motile activity by TGF-β1 and lidocaine was demonstrated with migration assay.

Results : Lidocaine was inhibited the proliferation of ARPE cells in concentration dependent manner after treatment of lidocaine, 24 hours and 48 hours, respectively. Migration activity of ARPE cells were inhibited by lidocaine and the migration of ARPE cells undergoing EMT by TGF-β1 was also inhibited significantly. Lidocaine prevented EMT by decreasing the activations of ERK, PI3K, Akt and smad, result in decreasing the expression of α-SMA, vimentin, and collagen I synthesis and increasing the expression of E-cadherin.

Conclusions : Lidocaine blocks the proliferation, migration, and EMT of ARPE cells by inhibition of TGF-β1 signaling pathway.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.


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