Fig. 1

PGAM5 is up-regulated in response to TBI A C57BL/6 J male mice were anesthetized and the dura mater of left hemisphere was exposed by a craniectomy. The sensorimotor cortex was impacted by CCI device at different velocity and deformation depth to mimic mild, moderate and severe TBI. B TTC staining and immunostaining of NeuN proteins of CCI mouse brains on 4 dpi. White dashed lines indicate the boundaries of the impacted lesion. Scale bar, 2 mm (upper) and 0.5 mm (bottom). C Immunoblot of PGAM5 in tissue lysate collected from left hemisphere on 4 dpi. D Quantification of relative PGAM5 levels normalized to GAPDH levels. Data are presented as mean ± SEM (n = 6). * p < 0.05, one‑way ANOVA with Tukey’s multiple comparisons. E Rat cortical neurons, hippocampal neurons and glia cells were isolated and cultured in vitro on DIV0. Primary neurons were scratch-injured with a pipette on DIV 8. Injured area was between the two black dashed lines. F Immunoblot of PGAM5 proteins in primary cortical neurons and glia cells. The numbers indicate the relative PGAM5 level normalized to GAPDH. Asterisk indicates the non-specific bands