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. 2019 Mar 26;10:326. doi: 10.3389/fphys.2019.00326

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Copyright © 2019 Drescher, Brandt, Fischer, Dreschers, Schwendener, Kowalska, Canbay, Wasmuth, Weiskirchen, Trautwein, Berres, Kroy and Sahin.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Serum PF4 is decreased in human patient samples and mice with acute liver disease. Serum levels of PF4 were decreased in patients with acute liver failure (ALF) when compared to healthy controls (ctrl) assessed by ELISA (A). In line, platelet numbers were decreased in humane blood samples (B). Immunofluorescent staining for CD41⁺ cells (CD41 (red), nuclei were counterstained with Dapi (blue), vessels are marked with white lines, magnification x200) (C). The quantitative evaluation shows that the platelet content within the liver of patients with ALF was increased compared to control (ctrl) (D). Comparable to the human situation, wild-type mice treated with GalN/LPS had reduced PF4 levels in serum (E) and decreased numbers of platelets in blood (F). Contrarily, the intrahepatic protein expression of PF4 was significantly increased when compared to control (ctrl) (G). This alteration was associated by augmented accumulation of platelets within the liver of wild-type mice (CD41 (red), Nuclei were counterstained with Dapi (blue), vessels are marked with white lines, magnification x200) (H) also shown in the quantitative analysis of the staining (I). n = 8, ^∗∗p < 0.01, ^∗∗∗p < 0.001.