Fig. 4: Akt2 cKO attenuates diabetes-induced increased protein level of EMT markers and decreased tight junction proteins in RPE. | Cell Death Discovery

Fig. 4: Akt2 cKO attenuates diabetes-induced increased protein level of EMT markers and decreased tight junction proteins in RPE.

From: Aberrant Akt2 signaling in the RPE may contribute to retinal fibrosis process in diabetic retinopathy

Fig. 4

A Representative RPE immunoblots and quantification of protein levels of EMT markers B Snail, C Twist1, D Vimentin, E adherens junction protein E-cadherin and F, G tight junction proteins ZO-1 and Occludin from 10 month old (8 months of diabetes) mice in Akt2fl/fl and Akt2 cKO RPE tissue. Diabetes significantly increased the levels of Snail, Twist1, and Vimentin, and decreased the levels of E-cadherin, ZO-1, and Occludin in the RPE cells from diabetic Akt2fl/fl mice compared to non-diabetic controls. However, Akt2 cKO significantly inhibited these diabetes-induced effects. n = 6 mice per group. Data are shown as Mean ± SD. *p < 0.05 and **p < 0.01. Statistical test used in this study is One-way ANOVA followed by Tukey’s post-hoc test. N non-diabetic, D diabetic, cKO conditional knock-out.

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