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Sohee Jeon, Won Ki Lee; Gli1 expression in human epiretinal membranes. Invest. Ophthalmol. Vis. Sci. 2017;58(8):3695.
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© ARVO (1962-2015); The Authors (2016-present)
To evaluate the expression of Gli1 in human epiretinal membranes (ERM) and to correlate this with clinical data.
A prospective, open-label, non-randomized, interventional study was done. Thirty-three human ERM specimens were immunolabeled with anti-Gli1 antibody and the number of total cells/hyperfield (HF), Gli1 (+) cells/HF, and the percentage of Gli1 (+) cells/total cells were calculated. We evaluated the interrelationship of cellular properties and clinical findings, such as presence of diabetic retinopathy (DR), retinal breaks, intraocular inflammation, central foveal thickness, maximal retinal thickness, retinal contraction, lamellar holes, pseudoholes, the attenuation or absence of an inner segment/outer segment (IS/OS) junction/external limiting membrane (ELM), cystic changes, and paravascular inner retinal defects.
Among 33 specimens, 25 specimens (75.8%) showed nuclear Gli1 expression. The mean Gli1 (+) cells/total cells was 54.0 ± 36.7% (range, 0–92.8%). There was significantly higher expression of Gli1 (+) cells in ERM specimens from patients with DR (p = 0.014), and lower expression from patients with retinal breaks (p = 0.022). ERM specimens from patients with OCT findings, such as intraretinal cysts, the absence of an IS/OS line, and the attenuation or absence of ELM, showed a significantly higher percentage of Gli1(+) cells/total cells (p = 0.001, p =0.001, p =0.002, and p =0.001, respectively).
Gli1 expression was detected in most ERM specimens. Patients who had diabetic retinopathy or OCT findings indicating chronic retinal insults showed higher Gli1 expression. Gli1 may have a role in the pathogenesis of ERM after chronic retinal insults.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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