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. 2021 Feb 15;131(4):e135296. doi: 10.1172/JCI135296

Figure 2. Sema3G is elevated in the vitreous of patients suffering from PDR.

Figure 2

(A) Angiography and SD-OCT were obtained from patients. Nonvascular ocular pathologies patients served as controls. Scale bars: 2000 μm (top), 500 μm (center). (B) ELISA assessment of vitreous fluid shows induction in Sema3G, IL-8, and VEGFA. The results are expressed as the absolute concentrations compared with control patients (n = 10 samples). (C and D) Immunoblot analysis and quantification of Sema3G protein levels in equal volumes of vitreous fluid from patients (n = 3 samples for each group). (E and F) Immunoblot analysis and quantification of Sema3G protein levels in equal volumes of aqueous humor from patients with PDR without DME, PDR with DME, and DME only (n = 3 samples for each group). Nondiabetic patients undergoing cataract surgery served as controls. (G) RNA in situ hybridization for Sema3G mRNA and immunofluorescence for lectin (an EC marker) in fibrovascular membranes (FVMs) of patients suffering from PDR. Error bars represent mean ± SEM, *P < 0.05; **P < 0.01; 2-tailed Student’s t tests (B and D), 1-way ANOVA with Tukey’s multiple comparisons test (F). Scale bar: 50 μm (G).