July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Expression of proteoglycan decorin in opacified posterior capsule and its suppression by TGFβ in mouse lens epithelial cells
Author Affiliations & Notes
  • Shinsuke Shibata
    Department of Ophthalmology, Kanazawa Medical University, Ishikawa, Japan
  • Naoko Shibata
    Department of Ophthalmology, Kanazawa Medical University, Ishikawa, Japan
  • Teppei Shibata
    Department of Ophthalmology, Kanazawa Medical University, Ishikawa, Japan
  • Hidetoshi Ishida
    Department of Ophthalmology, Kanazawa Medical University, Ishikawa, Japan
  • Etsuko Kiyokawa
    Department of Oncogenic Pathology, Kanazawa Medical University, Kahoku, Ishikawa, Japan
  • Hiroshi Sasaki
    Department of Ophthalmology, Kanazawa Medical University, Ishikawa, Japan
  • Eri Kubo
    Department of Ophthalmology, Kanazawa Medical University, Ishikawa, Japan
  • Footnotes
    Commercial Relationships   Shinsuke Shibata, None; Naoko Shibata, None; Teppei Shibata, None; Hidetoshi Ishida, None; Etsuko Kiyokawa, None; Hiroshi Sasaki, None; Eri Kubo, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 5636. doi:
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      Shinsuke Shibata, Naoko Shibata, Teppei Shibata, Hidetoshi Ishida, Etsuko Kiyokawa, Hiroshi Sasaki, Eri Kubo; Expression of proteoglycan decorin in opacified posterior capsule and its suppression by TGFβ in mouse lens epithelial cells. Invest. Ophthalmol. Vis. Sci. 2018;59(9):5636.

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

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Abstract

Purpose : Cytokines including TGFβ2 are involved in postoperative posterior capsule opacity (PCO). Previously, using a rat PCO model, we demonstrated that the expression of proteoglycan decorin (DCN) was highly up-regulated in lens epithelial cells (LEC). In the present study, we investigated DCN expression in a mouse PCO model and mouse LECs (MLECs) treated with TGFβ2 and/or its inhibitor.

Methods : All animal experiments adhered to the National Institutes of Health Guide for the Care and Use of Laboratory Animals. Extracapsular lens extraction (ECLE) was performed in C57/BL6 mice to generate the mouse PCO model. We used primary MLECs and peroxiredoxin 6 (Prdx6) deficient MLECs (Prdx6-/- MLEC) in which TGFβ is highly upregulated. MLECs reared in DMEM containing 2% fetal bovine serum were treated with 0 to 10ng/ml TGFβ2 and/or LY364947 and expression levels of DCN and α smooth muscle actin (αSMA) were measured using real-time RT-PCR.

Results : Expression of DCN, was upregulated at Day 7 after ECLE. After treatment with TGFβ2, expression of DCN was decreased, whereas, expression of Tpm1/2 and αSMA were upregulated in MLECs. Addition of TGFβ2 suppressed the expression of DCN mRNA (p<0.01). However, inhibition of TGFβ increased the expression of DCN. Expression of DCN was lower in Prdx6-/- MLECs than in wild type MLECs (p<0.02).

Conclusions : DCN may be involved in the progression of PCO. However, since expression of DCN was suppressed by TGF, DCN might not play a major role in the epithelial to mesenchymal transition of LEC in PCO. Further investigation is needed to clarify the involvement of DCN in the development of PCO in LEC.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

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