Fig. 8: Fpn1 knockout in ECs exacerbates glial hyperplasia and inhibits neuronal development during the long-term recovery period following ischemic stroke. | Cell Death & Disease

Fig. 8: Fpn1 knockout in ECs exacerbates glial hyperplasia and inhibits neuronal development during the long-term recovery period following ischemic stroke.

From: Cdh5-mediated Fpn1 deletion exerts neuroprotective effects during the acute phase and inhibitory effects during the recovery phase of ischemic stroke

Fig. 8

The distribution of GFAP (A), Ki67(B), DCX (C), and NeuN (D) in the cortex detected by immunofluorescence staining (scale bar = 50 μm). Quantification of immunofluorescence staining of GFAP (E), Ki67(F), DCX (G), and NeuN (H) (n = 4, unpaired t-test). The data are presented as the mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001.

Back to article page