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. 2023 Aug 4;21:286. doi: 10.1186/s12916-023-02959-8

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — CUS and CSF1Ri inhibited Csf1r and angiogenic genes in mice. (A) GO-BP enrichment analysis shows top-ranked pathways of DEGs derived from group comparisons. (B) Volcano plot shows these DEGs, which are colored in red if -Log₁₀ adj. p ≥ 1.3 and |Log₂FC| ≥ 0.2 and in blue if |Log₂FC| < 0.2. Angiogenic DEGs are highlighted by red dots with gene symbols when -Log₁₀ adj. p ≥ 3. (C) Heatmap shows 38 angiogenic DEGs. Downregulated (in purple frame) and upregulated (in orange frame) genes are highlighted in the heatmap. (D) mRNA expression of Csf1r and (E) mRNA expression of Pik3cg in the PFC (n = 7 mice per group). Ctr: Control; CUS: chronic unpredictable stress; CSF1Ri: CSF1R inhibitor; Veh: Vehicle. Data presented as mean ± SEM; **/*** p < 0.01/0.001 compared to Ctr-Veh. Two-way ANOVA with Bonferroni’s correction. See also Additional file 1: Tables S4 & S5 and Additional file 2: Fig. S2