Fig. 4: In vivo validation of the ALK5/VEGFC pathway. | Nature Cardiovascular Research

Fig. 4: In vivo validation of the ALK5/VEGFC pathway.

From: Human ocular fluid outflow on-chip reveals trabecular meshwork-mediated Schlemm’s canal endothelial dysfunction in steroid-induced glaucoma

Fig. 4

a, siRNA-mediated knockdown of ALK5 in vivo. Immunofluorescent staining of ALK5, Prox1 and DAPI 48 h after intracameral injection of scramble or ALK5 siRNA. b, Quantification of ALK5 signal normalized by DAPI (n = 8 and 11 FOVs in five mice, respectively). c, IOP measured in the steroid-induced mouse glaucoma model with or without ALK5 knockdown (n = 10 mice). d, AH mouse VEGFC concentration with or without ALK5 knockdown under DEX or DMSO treatment (n = 10, 9, 10 and 10 mice, respectively). e, Prox1 and VE-Cad staining of mouse SC endothelium in the steroid-induced glaucoma model with or without ALK5 knockdown. f, Junction widths of mouse SC endothelium in the steroid-induced glaucoma model with or without ALK5 knockdown (n = 8, 4, 6 and 5 mice, respectively). Scale bars, 100 μm (a) and 25 μm (e). All data are presented as mean ± s.d. Statistical comparisons were performed using unpaired two-sided Student’s t-tests in b; using one-way ANOVA with Tukey’s post hoc test (two-sided) in c,d,f. Exact P values are shown in bd,f.

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