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Fig. 4 | Fluids and Barriers of the CNS

Fig. 4

From: Microglia-derived CCL2 has a prime role in neocortex neuroinflammation

Fig. 4

Representative images of neocortex sections from naïve (a), EAE-affected (b; cs 2.0) and EAE-affected MSC-treated (c; cs 1.5) mice, sacrificed 24 h after MSC treatment, and double immunostained for GFAP and CCL2. a GFAP-reactive astrocytes are recognizable, scattered in the parenchyma (arrowheads) and concentrated perivascularly (arrows); note the CCL2 staining on the microvessel wall (V). b In EAE-affected mice, the neocortex is characterized by diffuse astrogliosis with hypertrophic astrocytes that express high levels of GFAP; the microvessels (V) are ensheathed by GFAP+ perivascular endfeet (arrows) together with CCL2+ microglia-like processes (arrowheads). c The condition shows recovery in EAE-affected MSC-treated mice, where GFAP+ perivascular astrocytes once again prevail on the vessel wall (V). TOPRO-3 nuclear counterstaining. Scale bars: a–c 25 µm

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