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JINGWEN YU, Shangkun Ou, Huimin Sun, Han Wu, Yuli Guo, Minjie Zhang, Zuguo Liu, Wei Li; FGF9 regulates endothelial-to-mesenchymal transition of corneal endothelial cells. Invest. Ophthalmol. Vis. Sci. 2019;60(9):5086. doi: https://doi.org/.
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Corneal endothelial cells (CECs) can undergo endothelial-to-mesenchymal transition (EndMT) after injuries or during ex vivo culture. Fibroblast growth factor 9 (FGF9) is reported to reverse the epithelial-to-mesenchymal transition in prostate cancer cells and accelerate wound healing. Our current study aims to investigate the expression and function of FGF9 on CECs.
The expressions of FGF9 and its receptor FGFR3 on CECs of human and rabbit were detected by immunohistochemistry and PCR. Slit-lamp microscope observation was performed on day 0, day 4 and day 7 after corneal endothelial injuries. Endothelial cells were harvested at different time points and the gene expressions of N-cadherin, ZO-1, Na+-K+ -ATPase, α-SMA, FGF9, and FGFR3 were detected by qRT-PCR. Rabbit CECs were cultured in SHEM for 4 passages with or without exogenous FGF9. CCK8 and immunofluorescence staining of N-cadherin, ZO-1, Na+-K+ -ATPase, α-SMA, FGF9, FGFR3, and Ki67 were performed on FGF9-treated CECs.
FGF9 and FGFR3 were expressed on both human and rabbit CECs. During rabbit corneal endothelium wound healing process and ex vivo culture, α-SMA was upregulated, while FGF9, FGFR3, N-cadherin, ZO-1, and Na+-K+ -ATPase were downregulated. Under the treatment of exogenous FGF9, α-SMA was down-regulated while FGF9, FGFR3, N-cadherin, ZO-1, and Na+-K+ -ATPase were upregulated in cultured CECs. Exogenous FGF9 had no effects on cell viability or proliferation.
FGF9 and its receptor FGFR3 are expressed on CECs. FGF9-FGFR3 signaling pathway is involved in the process of EndMT and phenotype transition of CECs.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.
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