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. 2019 Jun 25;16(3):466–485. doi: 10.1080/15548627.2019.1628538

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© 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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Figure 5. — PLA2G4A inhibition normalizes lysosomal membrane lipid composition and attenuates lysosomal membrane permeabilization after TBI.

(A-C) Comparison of positive ion mode UPLC-HDMS of lysosomal membrane prepared from the cortices of sham, TBI and TBI+AACOCF₃ using Partial Least Squares – Discriminate Analysis (PLS-DA) plot. Each point represents data set from an individual animal; sham (red), TBI (blue), TBI+AACOCF₃ (green). The 95% confidence intervals are indicated by elliptical shaded areas surrounding each group. (A) PLS-DA plot comparing Sham, TBI, and TBI+AACOCF₃ in positive ion mode UPLC-HDMS; R2 = 0.97, Q2 = 0.32. (B) PLS-DA plot comparing TBI and TBI+AACOCF₃ in positive ion mode UPLC-HDMS; R2 = 0.92, Q2 = 0.34. (C) PLS-DA plot comparing Sham and TBI+AACOCF₃ in positive ion mode UPLC-HDMS; R2 = 0.95, Q2 = 0.64. Data were sum normalized, log transformed, and mean centered. n = 4 animals/group. Plots generated using MetaboAnalyst. (D-F) Abundance of specific classes of phospholipids is normalized in the lysosomal membranes from AACOCF₃ treated TBI mice as compared to vehicle treated TBI controls. Individual data points as well as mean ± SEM are indicated. Sham (red), TBI (blue), and TBI+AACOCF3 (green). n = 4 animals/group. (D) LPC/LPE abundance. Calculated p-values for TBI to TBI+AACOCF₃ were 0.7124 (LPC(16:0)), 0.3140 (LPC(18:0)), and 0. 0366 (LPE(18:0)). (E) PC/PE abundance. Calculated p-values for TBI to TBI+AACOCF₃ were 0.0253 (PC(18:0/20:4)), 0.0224 (PC(18:0/22:6)), 0.0071 (PE(16:0/22:6)), and 0.0130 (PE(18:1/22:4)). (F) Ether PE abundance. Calculated p-values for TBI to TBI+AACOCF₃ were 0.0074 (PE(P-18:0/22:6)), 0.0020 (PE(P-18:0/20:4)), and 0.0209 (PE(P-18:0/22:6)). (G and H) Activity of lysosomal enzymes (G) NAGLU and (H) CTSD in the cytosolic fraction from sham and TBI mouse cortices. Data are mean ± SEM, n = 8–10 animals/group; *p < 0.05, **p < 0.01 (One-way ANOVA with Turkey’s multiple comparison test). (I-J) IF analysis demonstrating decreased cytoplasmic leakage of CTSL in TBI+AACOCF₃ as compared to TBI cortex. (I) Images (20×) of cortical brain sections from sham, sham+AACOCF₃, TBI and TBI+AACOCF3 mice stained with antibodies against neuronal marker RBFOX3/NeuN (green) and CTSL (red). Scale bar: 50 μm (J) Corresponding quantification of cells with diffused (cytosolic) CTSL staining. Data are mean ± SEM, n = 3 for vehicle or AACOCF₃ treated sham and 5 for vehicle or AACOCF₃ treated TBI mice; *p < 0.05, (Two-way ANOVA with Bonferroni posttests).