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. 2023 May 22;14:2900. doi: 10.1038/s41467-023-38624-0

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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 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/.

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Fig. 4 — a Principal Component Analysis (PCA) of 640 cytokines profiled with Quantibody (Quantitative Multiplex ELISA) arrays from TA muscle homogenates obtained from mice with or without platelet depletion at 1, 7, and 14 days from CTX-induced injury. Uninjured muscles after 7 days from platelet depletion were also analyzed. b Heatmap of 522 cytokines that are prominently regulated (based on the average z-scores) during muscle regeneration and/or in response to platelet depletion. c Cytokine categories that are collectively regulated at different timepoints of muscle regeneration in a platelet-dependent manner include cytokines that promote neutrophil chemotaxis (day 1 from injury) and the inflammatory response (day 7–14 from injury). See also Supplementary Fig. 5. d Chemokines that promote neutrophil chemotaxis peak at day 1 after injury but their levels are reduced by platelet depletion. The graphs display the mean ±SD with n = 4 biologically independent muscles from 4 independent mice for each timepoint and condition; *P < 0.05, **P < 0.01, ***P < 0.001 (unpaired two-tailed t test) refer to the comparison of muscles from control versus platelet-depleted mice at a given timepoint. e In vitro neutrophil chemotaxis assays with recombinant versions of platelet-secreted chemokines. CXCL5 and CXCL7 have the strongest chemoattractant activity. The graphs display the mean ±SD with n = 17 (buffer), n = 18 (rCXCL7), n = 18 (rCXCL5), n = 6 (rCXCL4) biologically independent samples; ***P < 0.001 (one-way ANOVA with Tukey post hoc test), ns = not significant. f Consistent with the cytokine array data in d, ELISA assays indicate that the total levels of CXCL7 increase in skeletal muscle upon injury. The graph displays the mean ±SD with n = 11 biologically independent samples; ***P < 0.0001 (unpaired two-tailed t test). g Additional ELISA assays with antibodies specific for inactive CXCL7 (i.e., which has not been proteolytically processed) indicate a decrease in inactive CXCL7 in injured muscles. The graph displays the mean ±SD with n = 11 biologically independent samples; ***P = 0.0004 (unpaired two-tailed t test). Together, these data indicate that the surge in total CXCL7 observed in injured muscles largely consists of proteolytically-cleaved (and hence active) CXCL7. Source data are provided in the Source data file.