Fig 2: Depletion of residual BM-Mfs impedes sinusoidal endothelial cell (SEC) regeneration. (A) In situ immunofluorescence showing bone marrow sinusoids (green, CD105) after 5-Gy irradiation. Nuclei were stained with DAPI (blue). (B) Immunofluorescence images of bone marrow sinusoids (green, CD105) at 3 days after 5-Gy irradiation in PBS controls and mice with Mfs depletion by Clo-lip. Scale bar, 50 µm. (C-H) Flow cytometry analysis to determine relative percentage of SECs (CD45-Ter119-CD31+CD105+) among BMNCs (C), number of SECs per femur (D), relative percentage of CD31+ ECs (CD45-Ter119-CD31+CD105-) among BMNCs (E), number of CD31+ ECs per femur (F), relative percentage of CD105+ stromal cells (CD45-Ter119-CD31-CD105+) among BMNCs (G) and number of CD105+ stromal cells per femur (H) at indicated times after 5-Gy irradiation and pretreatment with PBS- or Clo-lip injection (n = 3-6 mice). Data are shown as mean ± SD. *P < 0.05; **P < 0.01; ***P < 0.001 (t-test).

Fig 3: CSD causes brain vascular fibrinogen deposition and angiogenesis in a dose-dependent manner. a, Minimal detection of fibrinogen and angiogenesis markers (CD202, CD105, and VEGFR2) detected in brain vasculature of nonstressed mice. b, Perivascular fibrinogen deposition and angiogenesis in CSD exposed mouse. c, Example of a parenchymal fibrinogen leak surrounded by angiogenesis markers in a CSD brain. d, Perivascular fibrinogen accumulation with minimal angiogenesis in CSD exposed brain. e, CSD exposure causes significant fibrinogen deposits, and this occurs in a dose-dependent manner. f, Brain vascular angiogenesis increases with increasing CSD exposure. g,h, CSD-exposed mice showed significant declines in light:dark crosses (g), and social exploration (h) compared to nonstressed mice. Scale bar = 20 µm for (a,b) and 40 µm for (d,f). N = 5 for HC and CSD1, N = 6 for all other groups. One-way ANOVA: * p < 0.05, ** p < 0.01, *** p < 0.001.