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. 2022 Oct 13;13:6045. doi: 10.1038/s41467-022-33773-0

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — a Representative immunoblots and quantification of (b) phospho-Akt2, (c) total-Akt2, (d) phospho-Akt1 and (e) total Akt1 in RPE lysates obtained from diabetic and nondiabetic Akt2^fl/fl and cKO mice. Diabetes increased the level of phospho-Akt2 but did not affect the levels of total Akt2 in Akt2^fl/fl RPE cells compared to the nondiabetic control. RPE-specific Akt2 cKO reduced the levels of both phospho- and total-Akt2 in the RPE; induction of diabetes did not further affect the levels of either phospho- or total Akt2 in Akt2 cKO RPE. Induction of diabetes in Akt2^fl/fl mice decreased the level of phospho-Akt1 but did not affect the levels of total Akt1 in the RPE cells compared to nondiabetic control. Akt2 cKO increased the levels of phospho-Akt1 in diabetic Akt2 cKO mice, but not in nondiabetic cKO mice compared to diabetic or nondiabetic Akt2^fl/fl mice, respectively. The total Akt1 in the RPE was upregulated in both nondiabetic and diabetic Akt2 cKO mice compared to Akt2^fl/fl mice. f Representative immunoblots. g The ratio of phospho-GSK3β/total GSK3β was lower in diabetic Akt2^fl/fl mice, relative to nondiabetic control mice. However, it was increased in diabetic Akt2 cKO mice. h In addition, Akt2 cKO rescued the diabetes-induced increase in the ratio of p-NF-κB p65/total NF-κB p65. i Representative immunoblots. Diabetes induction increased the protein level of (j) ICAM-1 and (k) iNOS in Akt2^fl/fl mice, whereas in diabetic Akt2 cKO mice this diabetes-induced increase in inflammatory protein levels was significantly rescued. In (b–e, g, h, j, k), n = 6 mice per group, the data are expressed as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001 denotes changes versus Akt2^fl/fl nondiabetic (N) control. ^†p < 0.05, ^††p < 0.01, ^†††p < 0.001, and ^††††p < 0.0001 denotes changes with respect to Akt2^fl/fl diabetic (D) mice. ^###p < 0.001 and ^####p < 0.0001 shows changes versus nondiabetic Akt2 cKO group. Statistical test used in this study is One-way ANOVA followed by a Tukey’s post hoc test. Exact p values are: b p = 0.025 (Akt2 ^fl/fl D vs. Akt2 ^fl/fl N), p < 0.0001 (Akt2 cKO N vs. Akt2 ^fl/fl N, Akt2 cKO D vs. Akt2 ^fl/fl D). c p < 0.0001 (Akt2 cKO N vs. Akt2 ^fl/fl N, Akt2 cKO D vs. Akt2 ^fl/fl D). d p = 0.0109 (Akt2 ^fl/fl D vs. Akt2 ^fl/fl N), p = 0.0009 (Akt2 cKO D vs. Akt2 ^fl/fl N), p < 0.0001 (Akt2 cKO D vs. Akt2 ^fl/fl D), p = 0.0007 (Akt2 cKO D vs. Akt2 cKO N). e p = 0.0005 (Akt2 cKO N vs. Akt2 ^fl/fl N), p < 0.0001 (Akt2 cKO D vs. Akt2 ^fl/fl N). p < 0.0001 (Akt2 cKO D vs. Akt2 ^fl/fl D). g p = 0.0326 (Akt2 ^fl/fl D vs. Akt2 ^fl/fl N), p = 0.0001 (Akt2 cKO D vs. Akt2 cKO N), p < 0.0001 for the rest. h p = 0.0003 (Akt2 ^fl/fl D vs. Akt2 ^fl/fl N), p = 0.0283 (Akt2 cKO D vs. Akt2 ^fl/fl D). j p = 0.0004 (Akt2 ^fl/fl D vs. Akt2 ^fl/fl N), p = 0.011 (Akt2 cKO D vs. Akt2 ^fl/fl D). k p < 0.0001 (Akt2 ^fl/fl D vs. Akt2 ^fl/fl N), p = 0.0076 (Akt2 cKO D vs. Akt2 ^fl/fl D). Source Data is provided in the Source Data file.