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AIM:To identify transcriptional differences between the ocular surface ectoderm(OSE)and surface ectoderm(SE)using RNA-seq, and elucidate the OSE transcriptome landscape and the regulatory networks involved in its development.METHODS:OSE and SE cells were differentiated from human embryonic stem(hES)cells. Differentially expressed genes(DEGs)between OSE and SE were analyzed using RNA-seq. Based on the DEGs, we performed gene ontology(GO)analysis, Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analysis, and protein-protein interaction(PPI)network analysis. Transcription factors(TFs)and hub genes were screened. Subsequently, TF-gene and TF-miRNA regulatory networks were constructed using the NetworkAnalyst platform.RESULTS:A total of 4 182 DEGs were detected between OSE and SE cells, with 2 771 up-regulated and 1 411 down-regulated genes in OSE cells. GO-BP analysis revealed that up-regulated genes in OSE were enriched in the regulation of ion transmembrane transport, axon development, and modulation of chemical synaptic transmission. Down-regulated genes were primarily involved in nuclear division, chromosome segregation, and regulation of cell cycle phase transition. KEGG analysis indicated that up-regulated genes in OSE cells were enriched in signaling pathways such as cocaine addiction, axon guidance, and amphetamine addiction, while down-regulated genes were enriched in proteoglycans in cancer, ECM-receptor interaction, protein digestion and absorption, and cytokine-cytokine receptor interaction. Additionally, compared with SE, 204 TFs(including FOS, EGR1, POU5F1, SOX2, and PAX6)were up-regulated, and 80 TFs(including HAND2, HOXB6, HOXB5, HOXA5, and HOXB8)were down-regulated in OSE cells. Furthermore, we identified 6 up-regulated and 9 down-regulated hub genes in OSE cells, and constructed TF-gene and TF-miRNA regulatory networks based on these hub genes.CONCLUSIONS:The transcriptome characteristics of OSE and SE cells were elucidated through RNA-seq analysis. These findings may provide a novel insight for studies on the development and in vitro directed induction of OSE and corneal epithelial cells.
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@# ObjectiveTo discuss the effect of argon laser on retinal vein obstruction (RVO) . Methods428 eyes of 422 patients with RVO were treated by argon laser.Among them, there were 386 eyes with ischemic RVO,42 eyes with no-ischemic RVO, and 129 eyes with macular vesicular edema(MVE).ResultsThe vision acuity of 207 eyes is improved, and not changed in 138 eyes. The disappearing rate of MVE is 84.45%(82/97). ConclusionUsing argon laser to treat RVO can curb new vascular of retina building, lighten MVE and protect vision function.
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Aim To investigate the protective effect of erythropoietin(EPO )on neonatal rats'retinal neuronal cells injured by glutamic acid.Methods Retinal neuron cells were cultured and subjected to glutamic acid.The concentration of glutamic acid model was decided by observing the changes of neuronal cells with the releasing quantity of LDH and transmission electron microscope.Then cultured cells were divided into N group(normalcontral),G group(glutamic acid),EG group(EPO and glutamic acid),AG group(AG490 and glutamic acid),and AEG group(AG490,EPO and glutamic acid).MTT assay was applied to detect cell viability in five groups.The expression of Bax was detected with Western blot.Results The changes of mitochondrion and chromatin occurred in 50 ?mol?L-1 group and striking changes occurred in 100 ?mol?L-1 group with transmission electron microscope.There was apparent damage in 20?mol?L-1 group by the releasing quantity of LDH.MTT assay indicated the cell viability of EG group was higher than that of G,AG and AEG group,while,G group cell viability was higher than that of AG and AEG group.The expression of Bax in AG and AEG group was higher than that in G group. And that in G group was higher than in EG group.Conclusions EPO pretreatment can effectively protect the neuronal cells from injuries induced by glutamic acid.Down regulation of Bax and decrease of apoptosis through Jak2 passageway may be the mechanism of protection.