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. 2018 Feb 19;9(3):285. doi: 10.1038/s41419-017-0171-8

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© The Author(s) 2018

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 Cell viability analyses using MTT assay in H₂O₂ (50 μM for 1 h)-induced ONH astrocytes treated with Rp-cAMP (50 μM). b Cell viability analysis using MTT assay in H₂O₂ (50 μM)-induced ONH astrocytes transduced with AAV2/5-tdTomato or mCherry-PKI. Representative images showed tdTomato (red) or mCherry-PKI (red) expression in ONH astrocytes. Nuclei (blue) were stained by Hoechst 33342. Note that PKI overexpression promoted ONH astrocyte survival. Scale bars, 20 μm. c Immunoblot analyses of pAKT, total AKT, Bim and activated Bax in H₂O₂ (50 μM for 1 h)-induced ONH astrocytes transduced with AAV2/5-tdTomato or mCherry-PKI. d A hypothetical model for the role of tmAC activation-mediated cAMP/PKA signaling pathway in ONH astrocytes against glaucomatous insults such as elevated IOP and oxidative stress. For each determination, the cell viability as well as mRNA and protein expression in controls were normalized to a value of 1.0. Data are shown as the mean ± S.D. (n = 3). *P < 0.05; **P < 0.01; ***P < 0.001 (two-tailed unpaired Student’s t-test)