Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 May 1;11:2177. doi: 10.1038/s41467-020-15770-3

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2020

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/.

PMC Copyright notice

Fig. 7 — a Activated T cell CM (act-Tm) increased Iκbα phosphorylation in microglia, which was reduced following Caffeic acid phenethyl ester (CAPE; 100 µM) treatment. b CAPE treatment attenuated activated T cell CM (act-Tm)-mediated Ccl5 production in microglia. OPG o-GSCs were stimulated with Ccl5 at 300 pg ml⁻¹ for 3 days. Whereas no increased optic glioma stem cell (o-GSC) proliferation (%Ki67⁺ cells) was observed c, o-GSC apoptosis (%TUNEL⁺ cells) was reduced in the Ccl5-treated group compared to vehicle (Veh, 0.1% BSA) treated controls d. e Immunoblotting reveals activation of the Akt-GSK3β-CREB anti-apoptosis pathway following Ccl5 treatment, which was inhibited by AKT inhibitor (20 μM MK2206) treatment. f 20 μM MK2206 treatment inhibited the anti-apoptosis effect of Ccl5 on o-GSCs (%TUNEL⁺ cells). g Cd44 expression in o-GSCs was detected by qRT-PCR using splenocytes as a positive control. Cd44 expression differences were not statistically analyzed. h CD44 knockdown (CD44^KD) in o-GSCs reduces CD44 expression relative to the control shRNA-treated (Ctrl) cells. i Apoptosis (%TUNEL⁺ cells) of CD44^KDo-GSCs was not inhibited by Ccl5 treatment. j Immunoblotting reveals that Ccl5 activation of the Akt/GSK3β/CREB anti-apoptosis pathway was inhibited by CD44 knockdown. All data are presented as the mean ± SEM. b–d, f, i These representative experiments were conducted with b n = 3, c n = 6, d n = 5; f, i n = 4 independent biological samples and were replicated two additional times with similar results. g Bar graphs represent the means ± SEM of n = 3 independent biological samples. b–d, i Two-tailed Student’s t-test; f One-way ANOVA with Bonferroni post-test correction. Exact P values are indicated within each panel; N.S.; not significant. From left to right in each panel: b P = 0.001; c N.S.; d P = 0.003; f P = 0.003, N.S.; i P = 0.119. a, e, h, j These are representative images of n = 3 independent biological samples examined over three independent experiments with similar results. Molecular weight markers are denoted at the right side of each blot.