Fig. 7: Local inhibition of ADAM17 activity in the injured cortex promotes the differentiation of neuroblast to mature neurons. | Cell Death & Disease

Fig. 7: Local inhibition of ADAM17 activity in the injured cortex promotes the differentiation of neuroblast to mature neurons.

From: Specific inhibition of ADAM17/TACE promotes neurogenesis in the injured motor cortex

Fig. 7

Mechanical cortical lesions were unilaterally performed in the primary motor cortex of adult mice and locally injected with vehicle, an empty vector (both of them as controls) or Pro domain region of ADAM17 (ADAM17-Pro). Animals were sacrificed 28 days post-injury (s14+14 dpi), after receiving BrdU injections as explained in the figure. The upper right panel shows the experimental protocol for BrdU injection for s14+14 dpi mice, which were injected every 2 days for 14 days, and then sacrificed 14 days later, this is, 28 dpi. a Fluorescence microscopy images of the perilesional area showing proliferating BrdU+ cells (red), the green fluorescent protein ZS-Green, and the mature neuron marker NeuN (blue). b Graph shows the percentage of BrdU+ cells that coexpressed NeuN in the perilesional area. c Percentage of infected cells (expressing ZS-Green) that co-expressed BrdU and NeuN. Dotted lines delineate cortical lesion borders. d Image of an agarose electrophoresis gel showing the RT-PCR product of injury homogenates to detect ADAM17-Pro mutant in mice transduced with the ADAM17-Pro lentiviral vector (ADAM17-Pro); line 1 or the empty lentiviral vector (ZS-Green) line 2. −RT controls in lines 3 and 4. Scale bar = 100 and 50 µm in the high magnification picture. Data shown are the mean ± S.E.M.; n = 3–6 animals per group. Statistical analysis: ANOVA and Bonferroni posttest, *p < 0.05 when compared with rest of groups. L lesion

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