The generation of the GFAP-GFP mouse used in this study has been described previously (Zhou et al., 1997) and CD1 mice were obtained from Charles River Labs (Wilmington, MA). All mouse colonies were maintained in the animal facility of Children’s National Medical Center, and all animal procedures complied with the guidelines of the National Institute of Health, and with the Children’s Research Institute Institutional Animal Care and Use Committee (IACUC) guidelines. Male mice were placed in a chamber containing 10.5 ± 0.5% O2 from P3 to P11 as previously described (Ment et al., 1998 ; Fagel et al., 2006 (link)). Strain-matched and age-matched animals reared in normal oxygen levels were used as controls (normoxia). For studies examining proliferation, BrdU (Sigma; 50μg per gram body weight) was administered 2hr prior to sacrifice. Mice were sacrificed at the given time point after hypoxia and perfused transcardially with phosphate buffered saline followed by 4% paraformaldehyde (PFA) and post fixed overnight in PFA followed by 20% glycerol and stored at 4°C. Treatment of mice with the JAK/STAT inhibitor AG490 has been previously described (Zhou et al., 2011 (link); Xu et al., 2011 ). Briefly, CD1 mice were treated with AG490 (10 mg/kg i.p.) or DMSO (control) twice daily (injections were ~8–10 hours apart) from P6 to P11. At P11 the white matter was carefully dissected out and lysed as described below, followed by Western blot analysis.