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. 2021 Jan 13;41(2):251–268. doi: 10.1523/JNEUROSCI.0731-20.2020

Figure 1.

Figure 1.

HIFα stabilization in the early postnatal murine CNS. A, B, IHC of HIF1α and oligodendroglial lineage marker Sox10 in the spinal cord ventral white matter (Spc-WM, marked by dotted lines) of HIFα intact mice (A) and HIFα stabilized (Sox10-Cre:Vhlfl/fl) mice (B) at P5. C, D, IHC of HIF1α and Sox10 in the forebrain periventricular white matter (Fbr-PWM; marked by dotted lines) of HIFα intact mice (C) and HIFα stabilized (Sox10-Cre:Vhlfl/fl) mice (D) at P5. E, F, IHC of HIF1α and Sox10 in the Fbr-PWM of P10 mice that had been subjected to sham operation (E) and H/I injury on P6 (i.e., 4 d post-H/I or sham; F; for details, see Materials and Methods). Arrowheads in A–F point to HIF1α+Sox10+ cells. G, Western blot of microdissected subcortical white matter for HIF1α and canonical HIFα target PKM2 at 6 h post-H/I or sham. GAPDH, Internal loading control. H, PKM2 IHC in the Fbr-PWM at P10, 4 d post-H/I or sham. I1–I3, IHC and quantification of MBP staining in the Fbr-PWM at P10, 4 d post-H/I or sham. MBP intensity was normalized to that of the contralateral brain hemispheres to the occluded artery of the same mouse. Scale bars, 20 µm.