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. 2018 Jul 11;38(28):6247–6266. doi: 10.1523/JNEUROSCI.3017-17.2018

Figure 8.

Figure 8.

Inhibition of NOS3 upregulation in astrocytes protects oligodendrocytes and deletion of NOS3 promotes axon function against ischemia. A, MONs exposed to 60 min of OGD showed a progressive increase in NOS3 expression levels, which was attenuated with l-NIO (3 h following OGD: 3.8 ± 0.9% vs Control: 1.0 ± 0.1%), n = number of MONs. *p < 0.05, **p < 0.01; one-way ANOVA followed by Bonferonni's post hoc test. B, Colocalization of APC(+) oligodendrocytes, NOS3 (red), and Sytox (blue, nuclear staining) showed upregulation of NOS3 with OGD and loss of oligodendrocytes (white asterisks, right, merged). l-NIO (1 μm) application attenuated NOS3 upregulation and preserved oligodendrocytes. Scale bar, 5 μm. C, Colocalization of GFAP(+) astrocytes, NOS3 (red), and Sytox (blue, nuclear staining) showed upregulation of NOS3 mostly colocalized to activated astrocytic soma and processes (white arrows, right, merged). l-NIO (1 μm) application attenuated NOS3 upregulation in astrocytes and preserved oligodendrocytes. D, Axon function in MONs obtained from NOS3 knock-out mice showed improved axon function recovery following 60 min of OGD compared with control (WT) mice. n = number of MONs. ***p < 0.001; unpaired Student's two-tailed t test. E, Genotyping confirmation results for amplified DNA from tail samples. Note that the mutant band (NOS3−/−) was observed at 330 bp and the WT band (NOS3+/+) was observed at 337 bp on a 1.5% agarose gel.