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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Int+J+Ophthalmol
2018 ; 11
(7
): 1120-1128
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GSK3? inhibits epithelial-mesenchymal transition via the Wnt/?-catenin and
PI3K/Akt pathways
#MMPMID30046527
Zhang C
; Su L
; Huang L
; Song ZY
Int J Ophthalmol
2018[]; 11
(7
): 1120-1128
PMID30046527
show ga
AIM: To investigate the regulatory mechanism of glycogen synthase kinase 3?
(GSK3?) in epithelial-mesenchymal transition (EMT) process after proliferative
vitreoretinopathy (PVR) induction. METHODS: Experimental PVR was induced by
intravitreal injection of retinal pigment epithelium (RPE) cells in the eyes of
rabbits. A PI3K/Akt inhibitor (wortmannin) and a GSK3? inhibitor (LiCl) were also
injected at different time during PVR progress. Electroretinogram (ERG), ocular
fundus photographs, and B-scan ultrasonography were used to observe the PVR
progress. Western blot test on the extracted retina were performed at 1, 2, 4wk.
The expression of the mesenchymal marker vimentin was determined by
immunohistochemistry. Toxicity of wortmannin and LiCl were evaluated by ERG and
TdT-mediated dUTP nick-end labeling (TUNEL) assay. The vitreous was also
collected for metabolomic analysis. RESULTS: Experimental PVR could significantly
lead to EMT, along with the suppressed expression of GSK3? and the activation of
Wnt/?-catenin and PI3K/Akt pathways. It was verified that upregulating the
expression of GSK3? could effectively inhibit EMT process by suppressing
Wnt/?-catenin and PI3K/Akt pathways. CONCLUSION: GSK3? effectively inhibits EMT
via the Wnt/?-catenin and PI3K/Akt pathways. GSK3? may be regarded as a promising
target of experimental PVR inhibition.