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. 2021 May 5;11:9616. doi: 10.1038/s41598-021-89032-7

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© The Author(s) 2021

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/.

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PTX3, nPTX1, nPTX2 and PTX4 mRNA expression in lesioned brain areas. (A) PTX3 was upregulated in the ipsilateral cortex, striatum, hippocampus and thalamus early (24 h) and up to 2w (hippocampus) or 5w (cortex and striatum) after TBI compared to sham mice. (B) nPTX1 and PTX4 cortical expression were significantly increased 96 h after TBI and up to 1w (PTX4) compared to sham, while nPTX2 expression was uneffected. Data is presented as mean ± SEM, n = 6–8. For PTX3 in thalamus and nPTX1 and PTX4 in cortex computations assume that all rows are sampled from populations with the same scatter SD. Multiple t-test followed by Holm-Sidak post hoc test, *adjusted p < 0.05; **p < 0.01; ***p < 0.001 vs sham.