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Fig. 5 | BMC Neuroscience

Fig. 5

From: Col1a1+ perivascular cells in the brain are a source of retinoic acid following stroke

Fig. 5

Assessment of in vivo RA signaling activity. Spatial RA activity assayed using RARE-hsp68-LacZ mouse 7 days post 60 min MCAO injury. Confocal, tile-scan image of β-galactosidase immunolabeling (β-gal, green, A) with IB4 (magenta, A) at the level of the lesion (outlined with dashed line). A′ and A″ indicate magnified images in A. Tile stitched confocal images of RA activity in non-ischemic hemispheres (β-gal, green, B, C) and ischemic (β-gal, green, DE) with markers for neurons (NeuN, red, carets, B, D), astrocytes (GFAP, red, carets, C, E). Insets are magnified areas with dotted lines in D and E. Graphs depict quantification of NeuN+/β-gal+ neurons (F) and GFAP+/β-gal+ astrocytes (G) from non-ischemic and ischemic hemispheres 7 days following a 60 min MCAO (n ≥ 3 and bars represent SEM). Asterisks indicate statistically significant difference (p < 0.05) from uninjured/non-ischemic hemisphere and the ischemic hemisphere. PDGFrα + PSCs (red) in the non-ischemic cortex did not co-localize with β-gal (arrows, H) though β-gal+ cells are present in the granule cell layer of the dentate gyrus (DG) (carets, H). β-gal+ processes (green, I) appear to contact PDGFrβ+ PSCs (red) in the lesion core (open-arrows in I and I′) but PDGFrβ+ PSCs do not appear to co-label with β-gal (caret, I). β-gal+/PDGFrβ-negative cell bodies are adjacent to PDGFrβ+ PSCs (arrows, I). DAPI marks nuclei in blue. Scale bars 2 mm (A), 200 μm (B–E, I), 100 µm (H, I′)

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