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. 2011 Sep 28;32(2):353–367. doi: 10.1038/jcbfm.2011.136

Figure 6.

Figure 6

PDGFR-β deletion disrupts glial scar formation after cerebral ischemia. (A) Western blot analysis and (B) quantification of GFAP level in the ipsilateral (i) and contralateral cortices (c) of Floxed and Esr-KO mice after MCAO and sham-operated mice (n=3 per group). Each bar was normalized by GAPDH. Upper panel of (C) GFAP immunohistochemistry in Floxed and Esr-KO mice after MCAO. Scale bar=1 mm. Middle panel of panel C: schematic diagram of astrocyte density measurements. Lower panel of panel C: astrocyte density at different distances from the ischemic border in Floxed (n=6) and Esr-KO (n=7) mice at 14 days after MCAO. a2P<0.01 versus Floxed mice at the same distance from ischemic border. (D) Immunofluorescence stainings of GFAP in upper panel (green) and vimentin in lower panel (red), in Floxed and Esr-KO mice at 14 days after MCAO, counterstained with DAPI (blue). * indicates the ischemic core. Dotted lines indicate the ischemic border. Scale bar=20 μm. DAPI, 4′,6-diamidino-2-phenylindole; Esr-KO, PDGFR-β knockout mice; FITC, fluorescein isothiocyanate; GFAP, glial fibrillary acidic protein; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; MCAO, middle cerebral artery occlusion; PC/vSMC, pericyte/vascular smooth muscle cell; PDGFR, platelet-derived growth factor receptor.