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. 2021 Apr 15;162(10):2599–2612. doi: 10.1097/j.pain.0000000000002256

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Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the International Association for the Study of Pain.

This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

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Figure 4. — The DLK inhibitor IACS′8287 prevents transcriptome changes induced by cisplatin in the DRG. (A) Differentially expressed genes (DEGs) (padj<0.05) induced by cisplatin in comparison to PBS treatment and by IACS′8287 in cisplatin-treated mice. Venn diagram analysis shows that 582 genes were significantly altered in both comparisons. 740 genes were significantly altered only by cisplatin alone, whereas 1094 genes were significantly altered only by IACS′8287 in cisplatin-treated mice as compared to mice treated with cisplatin alone. (B) Heat map for the 2416 genes in (A) plotted using log2 fold changes induced by cisplatin and by IACS′8287 in cisplatin-treated mice. (C) Correlation plots for the log2 fold change of the 2416 genes induced by cisplatin and by IACS′8287 in cisplatin-treated mice. (D) Ingenuity pathway analysis of the 504 genes downregulated by cisplatin and upregulated by coadministration of IACS′8287. (E) Ingenuity pathway analysis of the 72 genes upregulated by cisplatin and downregulated by coadministration of IACS′8287. Results are expressed as mean ± SEM. DLK, dual leucine zipper kinase; DRG, dorsal root ganglion.