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 6
Microglia participate in retinal vascularization. Comparing C57BL/6J and BALB/cByJ strains revealed a difference in the number of CD11b⁺ microglia during the ischemic phase of OIR. (A) In whole mounts, both strains showed similar vaso-obliteration in the central retina at P12. However, at P17, there were dramatic differences in the vasculature, with C57BL/6J showing abundant neovascular tufts and little revascularization of the central retina. (B) C57BL/6J retinas contained fewer CD11b⁺ microglia over the course of 48 hours of ischemia compared with BALB/cByJ. The optic nerve head is positioned at the lower right in all images. (C) Quantification of CD11b⁺ microglia over time shows that C57BL/6J retinas had fewer microglia at P12 (0 hours) and less than half the number of microglia present in the retinas of BALB/cByJ mice at P14 (48 hours of ischemia). P ≤ 0.02 for BALB/cByJ versus C57BL/6J at all time points (n = 8–11). (D) Microglia depletion in C57BL/6J induced dramatic loss of preexisting microvasculature during retinal development. Injection of clodronate liposomes at P5 resulted in significant loss of CD11b⁺ microglia and capillary dropout at P8. Images depict similar locations in the central retina, with the optic nerve head at lower right. (E) Injection of clodronate liposomes into C57BL/6J at P2 caused significant depletion of CD11b⁺ microglia and dramatic disruption of the vasculature at P6 compared with control PBS liposome–treated fellow eye. Inset: Labeled liposomes (red) were taken up specifically by CD11b⁺ microglia (green) and not by GS lectin–labeled vascular cells (blue), nor any other CD11b^– cells. Magnification, ×4 (A and E, top panels), ×10 (D and E, bottom panels), ×20 (B), ×60 (E, inset).