Research Paper Volume 13, Issue 12 pp 16062—16071

PirB functions as an intrinsic suppressor in hippocampal neural stem cells

PirB knockout promotes NSC stemness maintenance. (A) PirB knockout (KO) was verified by western blot. Arrow: PirB molecular weight. (B–C) Neurospheres from wild-type and PirB-depleted animals indicate that PirB-deficient progenitors show an increased self-renewal capacity. (D) PirB depletion promoted cell proliferation. (E–F) PirB deficiency increased DNA synthesis in NSCs as shown by BrdU incorporation. Scale bar: 50 μm. (G) PirB knockout promoted cell cycle transition in NSCs, as measured by propidium iodide staining and flow cytometry. (H) 3,3’-diaminobenzidine (DAB) staining for PCNA shows the hippocampal dentate gyrus cell proliferation in 2- and 6-month-old mice, respectively. n ≥ 3. Means ± SEM, *P **P ***P t-test.

Figure 2. PirB knockout promotes NSC stemness maintenance. (A) PirB knockout (KO) was verified by western blot. Arrow: PirB molecular weight. (BC) Neurospheres from wild-type and PirB-depleted animals indicate that PirB-deficient progenitors show an increased self-renewal capacity. (D) PirB depletion promoted cell proliferation. (EF) PirB deficiency increased DNA synthesis in NSCs as shown by BrdU incorporation. Scale bar: 50 μm. (G) PirB knockout promoted cell cycle transition in NSCs, as measured by propidium iodide staining and flow cytometry. (H) 3,3’-diaminobenzidine (DAB) staining for PCNA shows the hippocampal dentate gyrus cell proliferation in 2- and 6-month-old mice, respectively. n ≥ 3. Means ± SEM, *P < 0.05; **P < 0.01; ***P < 0.001; ns = no significant difference by the t-test.