Myeloid progenitors differentiate into microglia and promote vascular repair in a model of ischemic retinopathy
J. Clin. Invest. Matthew R. Ritter, et al. 116:3266
doi:10.1172/JCI29683 [Go to this article.]

Figure 2
BM subpopulations accelerate retinal revascularization and reduce preretinal neovascular tuft formation in OIR. (AD) Computer-assisted image analysis was used to calculate the area of retinal vessel obliteration (yellow) and preretinal neovascular tuft formation (red) in whole mounts from OIR eyes at P17 (17). (E) Retinas treated with LinHSC prior to hyperoxia showed an almost 6-fold reduction in obliterated area versus uninjected controls and an approximately 5-fold reduction compared with vehicle-treated controls. (F) LinHSC treatment significantly reduced neovascular tufts compared with uninjected and vehicle-treated eyes. (G) LinHSCs reduced obliteration when administered prior to hyperoxia and during hyperoxia (P9 or P11) or just after return to normoxia (P12). inj, injected. (H) Mouse BM contained CD44hi and CD44lo fractions and the LinHSC population was enriched for CD44hi cells (red). Insets: Light-scattering properties of the CD44hi cells were typical of monocytes and granulocytes, while those of CD44lo cells were typical of lymphocytes. (I and J) Representative P17 retinas from eyes treated with CD44lo and CD44hi BM cells at P7. (K and L) Areas of obliteration (yellow) and neovascularization (red) at P17. When treated at P7, vascular obliteration (M) and neovascularization (N) were reduced in eyes treated with CD44hi cells with efficacy similar to eyes treated with LinHSC cells. Obliteration was similar between eyes treated with LinHSC and CD44hi cells, and neovascularization did not differ significantly between these groups (P = 0.25). Values represent mean ± SEM. *P < 10–5; **P ≤ 0.006. Magnification, ×4.