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A pterygium is an inflammatory, invasive and proliferative lesion on the ocular surface, which can decrease visual acuity, damage the ocular surface and affect the appearance of the eye. However, the underlying molecular mechanisms of the pathogenesis remain unclear. In the present study, the role of apoptosis-associated protein Livin in the occurrence and development of pterygium was investigated. Primary samples from quiescent or advanced clinical stages of pterygium and normal human conjunctival tissues were used to assess mRNA and protein expression levels of Livin using reverse transcription-quantitative PCR and immunohistochemistry, respectively. Livin was knocked down in pterygium epithelial cells (PECs) using small interfering RNA (siRNA), to investigate the role of Livin in PEC viability, migration, invasion ability and apoptosis. The cell viability, invasion ability and apoptosis of PECs following ultraviolet B (UVB) radiation alone or in combination with Livin silencing were also analyzed. Expression levels of Livin increased in the pterygium tissues compared with those in the normal conjunctiva at both the mRNA and protein levels. Livin expression levels in advanced pterygium were significantly higher compared with those in quiescent pterygium samples. Knockdown of Livin expression levels significantly reduced cell migration, invasion ability and cell viability, and induced apoptosis of PECs. Inhibition of Livin expression in PECs increased the expression levels of caspase-7, caspase-3 and E-cadherin, whereas expression levels of Snail were downregulated. Cell viability and invasion ability in PECs was enhanced following UVB radiation and Livin expression upregulated. UVB irradiation induced cell invasion ability of PECs and this was attenuated by Livin-silencing. Transfection with Livin siRNA also partially recovered the apoptosis rate of PECs, which was reduced by UVB irradiation. In conclusion, Livin was upregulated in pterygium, and UVB radiation functions in the development of pterygium by inducing Livin expression.

Background: Growing evidence reveals that circular RNAs (circRNAs) play roles in cancer development. However, the effects and possible mechanisms of circRNAs in retinoblastoma (RB) are far from clear. Methods: circVAPA expression pattern was identified by RT-qPCR. circVAPA induced effects on RB cells were tested by CCK-8, clone forming, flow cytometry and transwell assays. Bioinformatics assay, rescue experiments and dual-luciferase tests were applied for mechanism exploration. Additionally, mouse models were established for in vivo assays. Results: circVAPA was upregulated in human RB specimen and RB cell lines, and was correlated with poor outcomes of Rb patients. Knockdown of circVAPA could suppress the malignant phenotypes of RB. Mechanistic experiments demonstrated that miR-615-3p could reverse the circVAPA induced effects on RB cells, and the downstream oncogene SMARCE1 was positively regulated by circVAPA via miR-615-3p. Further, in vivo analysis confirmed the findings. Conclusion: In summary, circVAPA promoted RB proliferation and metastasis by sponging miR-615-3p, thereby upregulating SMARCE1. CircVAPA was a potential biomarker for Rb therapy.

AimTo investigate the changes in macular vessel density (mVD) and its relationship to macular ganglion cell–inner plexiform layer (mGCIPL) thickness in patients receiving ethambutol (EMB) therapy for tuberculosis without recognisable clinical symptoms or signs of EMB-induced optic neuropathy (EON).MethodsA total of 23 eyes of 13 patients using EMB therapy for 6 months without EON (preclinical EON) as the EMB group, 40 eyes of 23 healthy individuals as the normal control group and 18 eyes of 10 patients with tuberculosis before receiving EMB therapy as the blank control group were retrospectively analysed. The mean peripapillary retinal nerve fibre layer (pRNFL) and mGCIPL thicknesses and mVD were measured using optical coherence tomography angiography. Patients in the EMB group were compared with individuals in the normal and blank control groups, and changes in macular parameters were evaluated.ResultsCentral circle mVD (cCVD) was significantly lower in the EMB group than in both control groups (generalised estimating equation (GEE), p=0.003 and 0.029, respectively). The mGCIPL thickness in all regions and the mean pRNFL thickness were not significantly different between the EMB group and both control groups (GEE, p=1.000 for all). There were no significant differences in mVD, mGCIPL thickness and mean pRNFL thickness between the normal control and blank control groups (p>0.05). In the generalised linear model analyses, the minimum and inferonasal mGCIPL thicknesses were positively correlated with cCVD in the EMB group (β=1.285, p=0.003 and β=0.770, p=0.024, respectively).ConclusionscCVD decreased with no changes in mGCIPL and mean pRNFL thicknesses in patients with preclinical EON. The minimum and inferonasal mGCIPL thicknesses were positively correlated with cCVD. cCVD might be an early indicator for monitoring early-stage EMB toxicity.