(A–D) Deletion of NFIA resulted in decreased Thbs4 mRNA expression within the RMS and SVZ regions. (E) Quantification of Thbs4 ISH signal within the RMS and SVZ regions in NFIA^fl/+ GFAP-CreER versus NFIA^fl/fl GFAP-CreER mice. Quantification was performed by analyzing 8 sections per animal and 3 mice per genotype. Data are shown with box and whisker plots. The bounds of the boxes represent upper and lower quartiles, the lines in the boxes represent the median, and the whiskers represent the maximum and minimal values. **P = 0.000053 (RMS) and **P = 0.0000026 (SVZ), by Student’s t test. (F) Illustration of the prospective NFIA-binding site 240 bp upstream of the Thbs4 transcriptional start site and alignment with the consensus NFIA-binding sequence. (G) Anti-IgG and anti-NFIA antibodies were used to immunoprecipitate DNA fragments from cultured astrocytes. Fragments were analyzed via PCR using primers designed to include the prospective NFIA-binding site within the Thbs4 promoter region and showed that NFIA bound this predicted site. (H) Increasing concentrations of NFIA resulted in an increased activation of a luciferase reporter plasmid containing the Thbs4 promoter region when cotransfected in P19 cells. Data are shown as box-and-whisker plots. The bounds of the boxes represent upper and lower quartiles, the lines in the boxes represent the median, and the whiskers represent the maximum and minimal values. (I–K) Fluorescence immunostaining for NFIA combined with fluorescence ISH labeling for Thbs4 indicated coexpression within human neonatal HIE tissue. Solid white arrowheads show colabeling of Thbs4 and NFIA. Images in I–K are representative of tissue samples from 3 individual patients, 8 sections per patient. Scale bars: 50 μm (A–D and I–K).