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

Figure 1.

Figure 1

Experimental Plan. (A) WT mice underwent TBI or sham operation. TBI mice were sacrificed at different time points after surgery and plasma, whole brain or brain areas including cortex, striatum, thalamus and hippocampus were collected. PTX3 plasmatic levels were measured by ELISAs (naive; sham: 24 h, 5w; TBI: 30′, 24 h, 48 h, 96 h, 1w, 2w, 3w, 5w). PTX3 presence (sham: 5w; TBI: 30′, 24 h, 48 h, 96 h, 1w, 2w, 3w, 4w, 5w) and co-localization with neutrophils (Elastase; 48 h), neurons (NeuN; 1w), astrocytes (GFAP; 1w), microglia (CD11b; 1w), endothelial cells (CD31; 1w) and fibrin(ogen) (1w,2w) was studied by immunofluorescence assay on perfused brains. nPTX1, nPTX2, PTX3, PTX4 gene expression analysis was done on snap frozen brain areas by RT-qPCR (sham: 24 h, 96 h, 1w, 2w, 5w; TBI: 24 h, 96 h, 1w, 2w, 5w). (B) WT or PTX3 KO underwent CCI or sham operation. Sensorimotor deficits were assessed by composite neuroscore and beam walk tests on a weekly basis for four weeks after TBI. Brains from both strains were harvested for histopathological analysis: lesion volume and neuronal density with cresyl violet staining (1w; 5w); collagen presence with sirius red staining (5w); contra-lateral white matter loss with luxol fast blue staining (5w); astrogliosis (GFAP; 5w), microgliosis (CD11b/CD68; 5w) and shape descriptors microglia (CD11b; 1w) with immunohistochemistry.