Figure 9.

Deletion of HtrA1 does not alter vascular or immune cell morphology or distribution in the young-adult mouse neocortex. A, Representative micrographs illustrating the overall distribution and density of neurovascular unit components marked by GFAP (green), CD31 (red), and PDGFRβ (blue) in 6-month-old HtrA1 control (n = 6) and null mutant cortex (n = 4). B–D, Graphs showing the integrated density quantification of astrocytes (B; GFAP⁺ cells) and endothelial cells (C; CD31⁺ cells), as well as pericyte numbers (D; PDGFRβ⁺ cells) in HtrA1 control and null mutant cortex. E, Quantification of blood vessel properties in the cerebral cortex of 6-month-old adult HtrA1^+/+ and HtrA1^−/− mice. CD31 IHC signal was used to measure vessel properties listed on the y-axis of each graph. No significant differences were detected between HtrA1 mutant (n = 6) and control (n = 4) mice. F, Representative images of microglia markers CD11b (red) and Iba1 (green) in HtrA1 control and mutant mouse cortex. No significant differences were observed, suggesting HtrA1 deletion does not induce inflammatory responses in the uninjured adult mouse forebrain. Scale bar, 50 μm. *p ≤ 0.05.