July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Caveolin-1 downregulates glial fibrillary acidic protein and vimentin expression of mouse retina and cultured human Muller cell in pathology of proliferative vitreoretinopathy.
Author Affiliations & Notes
  • Yosuke Nagasaka
    ophthalmology, Nagoya univercity graduated school of medicine, Nagoya, Japan
  • Hiroki Kaneko
    ophthalmology, Nagoya univercity graduated school of medicine, Nagoya, Japan
  • Hiroko Terasaki
    ophthalmology, Nagoya univercity graduated school of medicine, Nagoya, Japan
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 5257. doi:
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      Yosuke Nagasaka, Hiroki Kaneko, Hiroko Terasaki; Caveolin-1 downregulates glial fibrillary acidic protein and vimentin expression of mouse retina and cultured human Muller cell in pathology of proliferative vitreoretinopathy.. Invest. Ophthalmol. Vis. Sci. 2018;59(9):5257.

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

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Abstract

Purpose : We previously reported caveolin-1, an integral membrane protein, blocks epithelial-mesenchymal transition of retinal pigment epithelial (RPE) cells and caveolin-1 knock out (Cav-1-/-) mouse develops severer proliferative vitreoretinopathy (PVR) after surgically induced retinal detachment (IOVS 2017). Muller glia is a major component of PVR and interaction with RPE cells is well known in PVR pathogenesis. Glial fibrillary acidic protein (GFAP) and vimentin are upregulated in the retina after retinal detachment and known to be important progenitor for fibrotic changes of Muller glial cells. Caveolin-1 is also reported to be rich in Muller cells. We investigate the role of caveolin-1 for GFAP and vimentin expression in the PVR pathogenesis.

Methods : PVR was induced surgically on the eyes of wild-type (WT) C57BL/6J and Cav-1-/- mice previously described. The cryo-sections of the PVR retina from both mice were immuno-stained with anti-GFAP and anti-vimentin antibodies and compared those expressions in the inner-retina of each mouse. Furthermore, to test the involvement of caveolin-1 role of human Muller cell in vimentin expression, MIO-M1 cells were co-cultured with human primary RPE cells using 0.4μm pore transwell insert, after transfection of siRNA_Cav-1 (siCav-1). Five days after co-culture, immunofluorescences of vimentin expression were observed microscopically.

Results : GFAP and vimentin expression were higher in the PVR retina from Cav-1-/- mice than C57BL/6J. The morphologies of MIO-M1 cells co-cultured with RPE cells were significantly different from single cultured cells. In co-cultured MIO-M1 cells transfected with siCav-1, relatively higher vimentin expression and morphologically changed cells were observed.

Conclusions : The retinal sections of Cav-1-/- mice showed higher GFAP and vimentin expression suggesting severer retinal gliosis. The immunofluorescence of co-cultured Muller cells showed larger number of higher expression of vimentin and morphological change in the group of siCav-1 transfection. This finding can be pathological contribution of Muller cell to PVR pathogenesis.

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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