Figure 7: Transplantation of oxygen-glucose deprivation (OGD)-preconditioned microglia promotes angiogenesis in the border area within the ischemic core and axonal outgrowth in the ischemic penumbra at 28 days after cerebral ischemia.
From: Microglia preconditioned by oxygen-glucose deprivation promote functional recovery in ischemic rats
(A) Representative figures and bar graphs representing immunoreactivity for CD31 volume per unit volume, expressed as μm3 per μm3, in the ischemic core and penumbra from cerebral cortices of the no cell control group, OGD-astrocyte, or OGD-microglia transplanted groups at 28 days after cerebral ischemia. The cluster of differentiation (CD31; green)/4′,6′-diamidino-2-phenylindole (DAPI; blue) double labelling in the ischemic cortices at 28 days after cerebral ischemia as examined by confocal microscopy. Scale bars, 15 μm. (B) Representative figures and bar graphs representing immunoreactivity for SMI31 and MAP2-positive volumes per unit volume, expressed as μm3 per μm3, in the ischemic penumbra from the cerebral cortices of the no cell control group and OGD-preconditioned astrocyte or OGD-preconditioned microglia transplanted groups at 28 days after cerebral ischemia. SMI31 (green) or microtubule-associated protein 2 (MAP2; red)/DAPI (blue) double labelling in the ischemic cortices at 28 days after cerebral ischemia as examined by confocal microscopy. Scale bars, 7 μm. (C) Representative figures and bar graphs representing the relative signal intensities of chondroitin sulphate proteoglycan/neuron-glial antigen 2 (CSPG/NG2; green) from the cerebral cortices of the no cell control group and the OGD-preconditioned astrocyte or OGD-preconditioned microglia transplanted groups at 28 days after cerebral ischemia. CSPG/NG2 (green)/DAPI (blue) double labelling of the cerebral cortices in the ischemic penumbra at 28 days after cerebral ischemia as examined by confocal microscopy. Scale bars, 15 μm. The graph represents the relative signal intensities of the microglia or astrocytes transplanted into ischemic brain samples compared with samples from the no cell control group (N = 21–28). The bar graph represents the relative ratio of the signal intensities of the ischemic brain samples compared with that of sham-operated rat samples (N = 21–28). Moreover, a secondary-only antibody control confirms its specificity. *P < 0.05, **P < 0.01.
