June 2022
Volume 63, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2022
Extracellular Matrix Protein Periostin Regulates Epithelial Mesenchymal Transition of Lens Epithelial Cells
Author Affiliations & Notes
  • LAN ZHANG
    Zhongshan Ophthalmic Center, Sun Yat-sen University, China
  • David W Li
    Zhongshan Ophthalmic Center, Sun Yat-sen University, China
  • Footnotes
    Commercial Relationships   LAN ZHANG None; David Li None
  • Footnotes
    Support   NSFC#81970787, #82000876, #81770910, NSF-Guangdong Province and Guangzhou City Joint Program#20191515120014, ZOC-SKLO#3030901010110
Investigative Ophthalmology & Visual Science June 2022, Vol.63, 4045 – F0009. doi:
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    • Get Citation

      LAN ZHANG, David W Li; Extracellular Matrix Protein Periostin Regulates Epithelial Mesenchymal Transition of Lens Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2022;63(7):4045 – F0009.

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

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Abstract

Purpose : Epithelial mesenchymal transition (EMT) of lens epithelial cells (LECs) is one of the most important pathogenic mechanisms in lens fibrotic disorders such as anterior subcapsular cataract (ASC) and posterior capsule opacification (PCO). We recently showed that AKT-EZH2-H3K27me3 axis regulates the activation of mesenchymal genes during lens fibrosis. In the present study, we demonstrated that an important extracellular matrix (ECM) gene POSTN plays an essential role in lens EMT.

Methods : All experiments were based on injury induced ASC mouse model and TGF β-induced EMT of human lens epithelial cells. Quantitative real-time PCR, Digital Droplet PCR, Western Blot, and whole-mount immunofluoresce were used to examine the differential EMT gene expression.

Results : The ECM protein coding gene POSTN was upregulated in TGFβ-induced EMT of human lens epithelial cells, and in the lens capsule of injury-induced ASC mouse model as well as human ASC patients. POSTN gene silencing led to attenuated expression of EMT marker genes in TGFβ-induced EMT of human lens epithelial cells, which can be partially rescued by AKT1 overexpression. Moreover, POSTN knockout using CRIPSR-Cas9 technology in mouse led to suppressed expression of EMT marker genes and ASC plaque formation after injury-induced ASC procedure.

Conclusions : The present study demonstrated that the ECM gene POSTN plays an important role in regulating lens fibrosis. Mechanistically, the TGFβ-AKT–EZH2-H3K27me3 signaling axis activates POSTN expression, and in turn, though the activation of Integrin-AKT signaling, Periostin, encoded by POSTN, controls the activation of mesenchymal genes in lens epithelial cells. Thereby, Periostin participates in a feed-forward EMT signaling cascade, contributing to lens fibrosis. Intervention of important activated ECM genes such as POSTN may present a novel strategy for the prevention of lens fibrosis diseases. Supported by NSFC#81970787, #82000876, #81770910, NSF-Guangdong Province and Guangzhou City Joint Program#20191515120014, ZOC-SKLO#3030901010110.

This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.

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