Background Retinal neovascularization (NV) is a major cause of blindness in ischemic retinopathies and cell-based therapy represents an emerging approach to correct the underlying vascular abnormalities. Microglia and its progenitor were suggested to play great role in stabilizing and facilitating vascular repair, but there is problems about the cell transplantation. Macrophage-conlony stimulating factor is the main regulator of proliferation and activation of microglia. Here we investigated whether more activated microglia, produced by stimulation of M-CSF, can accelerate the revascularization and NV regression in oxygen-induced retinopathy (OIR).
Methods C57/BL6 mice were exposed to 75%±2% oxygen (P7-P12) and received intraperitoneal injection of M-CSF at post-natal day 12 (P12). Clodronate liposomes were injected into the peritoneal cavity and vitreous of mice at P12 to eliminate retinal microglia. The eyes were collected at P15, P17, and P21 to analyze the retinal microglia and revascularization. Western blot, RT-PCR and immnunochemistry was applied to evaluate the retina M-CSF, CSF-1R and CD11b (marker of microglia).
Results Retinal microglia made up a net between the vascular, providing connections. In OIR, microglia became activated and reduced at early phase and increased at late phase. Intraperitoneal injection of M-CSF could induce retinal microglia proliferation at early phase, more amoeboid-like microglia located along the main blood vessel and was found in larger density in the NV area to facilitated normalization of the vasculature. The process of revascularization and NV regression were accelerated in the OIR with M-CSF injection.
Conclusion Retinal microglia can proliferated through being stimulated by M-CSF and promote the process of revascularization and NV regression in OIR model. |
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