Abstract
BackgroundRetinal neovascularization has been intensively investigated in the mouse model of oxygen-induced retinopathy (OIR). Here, we studied the contribution of microglial cells to vascular regression during the hyperoxic phase and to retinal neovascularization during the hypoxic phase.MethodsMice expressing green fluorescent protein (GFP) under the Cx3cr1 promoter labeling microglial cells were kept in 75% oxygen from postnatal day 7 (P7) to P12. Microglial cell density was quantified at different time points and at different retinal positions in retinal flat mounts. Microglial activation was determined by the switch from ramified to amoeboid cell morphology which correlated with the switch from lectin negative to lectin positive staining of GFP positive cells.ResultsMicroglial cell density was constant in the peripheral region of the retina. In the deep vascular layer of the central region, however, it declined 14 fold from P12 to P14 and recovered afterwards. Activated microglial cells were found in the superficial layer of the central avascular zone from P8 to P12 and from P16 to P18. In addition, hyalocytes were found in the vitreal layer in the central region and their cell density decreased over time.ConclusionDensity of microglial cells does not correlate with vascular obliteration or revascularization. But the time course of the activation of microglia indicates that they may be involved in retinal neovascularization during the hypoxic phase.
Highlights
Retinal neovascularization has been intensively investigated in the mouse model of oxygen-induced retinopathy (OIR)
In the OIR mouse model, normal vascular development is interrupted when mice are being placed in hyperoxia (75% oxygen) from postnatal day 7 (P7) to P12
Our results demonstrate that increased numbers of activated microglial cells are found both during the hyperoxic phase from postnatal day 8 (P8) to P12 when retinal vaso-obliteration occurs and in the late hypoxic phase from P16 to P18 when pathological NV reaches its maximal severity and regresses
Summary
Retinal neovascularization has been intensively investigated in the mouse model of oxygen-induced retinopathy (OIR). In the OIR (oxygen-induced retinopathy) mouse model, normal vascular development is interrupted when mice are being placed in hyperoxia (75% oxygen) from P7 to P12. During this time, a large avascular zone is formed by loss of small caliber vessels in the central retina [2]. Hypoxic astroglial and neuronal cells in this region upregulate hypoxia-regulated growth factors to induce neovessel formation. Unregulated neovessel growth leads to funtional revascularization and induces pathological neovascularization (NV) in the inner retina [3]. Starting at P17, NV tufts and clusters begin to regress leading to a morphologically normal retinal vascular system around P25 [4]
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