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. Author manuscript; available in PMC: 2014 May 1.
Published in final edited form as: Neurobiol Aging. 2012 Dec 27;34(5):1397–1411. doi: 10.1016/j.neurobiolaging.2012.11.013

Figure 3. MHC II is expressed on MG/MΦ in the aged TBI brain.

Figure 3

(A) Quantitative real-time PCR was used to assess the expression levels of MHC II mRNA in cortical tissue from young (3 month) and aged (24 month) mice at 24 h post-injury. MHC II mRNA was significantly increased in the cortex of aged TBI brain when compared to the young TBI brain (p<0.05). Statistical analysis was by two-way ANOVA (injury x aging), followed by post-hoc adjustments using Student-Newman-Keuls Multiple Comparison test; *p<0.05, #p<0.05, where * = TBI 24 month vs. sham 24 month, # = TBI 3 month vs. TBI 24 month. Bars represent mean ± s.e.m. (B) Immunohistochemistry for MHC II in the thalamus of young and aged TBI mice at 7 d post-injury. MHC II immunoreactivity was detected in cells that displayed a ramified/hypertrophic-like MG/MΦ cellular morphology in ventrolateral thalamic subregions of the young TBI brain (i and iii). In contrast, intense MHC II immunoreactivity was detected in cells that displayed hypertrophic/bushy-like MG/MΦ cellular morphologies in the ventrolateral thalamus of aged TBI brain (ii and iv). Bar = 200μm, inset ii bar = 50μm, inset iv bar = 10μm. (C) Triple immunofluorescence staining for Iba-1 (green), MHC II (red) and ED1 (magenta) in the thalamus of young and aged TBI mice at 7 d post injury. In contrast to the young TBI brain MHC II was highly expressed in Iba-1/ED1-positive MG/MΦ in the aged TBI brain. Bar = 20μm.