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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Fibrin promotes oxidative stress and neuronal loss in traumatic brain injury via innate immune activation

Fig. 1

Fibrin(ogen) deposition in human and mice TBI. (A, B) Images from human brain tissue less than one day after TBI (A) and one year after injury (B), labeled for fibrin(ogen) (blue) and CD68 (brown). CD68 + cells (Δ) are present in areas with extravasated fibrin(ogen) (right panel), while not detected in areas without fibrin(ogen) (left panel). Scale bars, 100 μm. (C) Images from human brain one year after TBI, stained for fibrin(ogen) (blue) and Iba1 (brown). Amoeboid microglia (Δ) are present adjacent to parenchymal fibrin(ogen) deposits (right panel), while they are not detected in areas without fibrin(ogen) (left panel). Scale bar, 50 μm. (D) Images from human brain one year after TBI, stained for fibrin(ogen) (brown) and monocytes (MRP14, blue). MRP14+ monocytes (^) are present in areas adjacent to dense fibrin(ogen) deposits (brown) (right panel), while they are not detected in areas without fibrin(ogen) (left panel). Scale bar, 50 μm. (E) 3-D volume projection of a coronal view of a mouse brain with 2 MDa Dextran-casted vessels (green) and Alexa647-fibrinogen (red) 2-days after CCI. Representative of n = 3 mice. Scale bar, 1 mm. (F) (Left) Representative coronal images of peri-lesional mouse cortex stained for fibrin(ogen) (red) at 2 and 28 days post-injury (DPI). Scale bar, 500 μm. (Right) Quantification of fibrin(ogen) intensity in peri-lesional cortex relative to uninjured, contralateral cortex at multiple timepoints after CCI (red) or sham surgery (gray). Data are presented as mean ± s.e.m.; ***P < 0.001, ****P < 0.0001 determined by one-way ANOVA with Dunnett’s test for multiple comparisons; n = 4–7 mice per timepoint, each point is one mouse)

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