Fig. 4: HBEGF-TNF induces reactive gliosis, glial proliferation, and retinal dyslamination in HRO. | Nature Communications

Fig. 4: HBEGF-TNF induces reactive gliosis, glial proliferation, and retinal dyslamination in HRO.

From: HBEGF-TNF induce a complex outer retinal pathology with photoreceptor cell extrusion in human organoids

Fig. 4

a Schematic of photoreceptor and glial pathologic changes (10-days HBEGF-TNF (HT) treatment). b–e Immunostained serial HRO sections were used to quantify the level of gliosis (GFAP) as well as the photoreceptor cells (RCVRN), Müller glia (RLBP1/SLC1A3 costain), cell nuclei (DAPI) based on marker area analysis, and proliferating (KI67), mitotic (PHH3, phosphohistone H3), and SOX9-positive (Müller glia) cells based on cell counts. Graphs: circles show individual HROs (n) with n ≥ 5 per independent experiment (N, N = 4). Two-sided Student’s t test; *P < 0.0001. f Cell delamination was quantified to describe retinal dyslamination in HT-HROs compared to controls. Based on n ≥ 5 HROs (n) per independent experiment (N, N = 4). c, d, f Graphs (mean ± SD) and statistics over n. Scale bars: b, e serial reconstructions 1 mm, others 50 µm. See Supplementary Data 2. Source data are provided as a Source Data file.

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