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Fig. 3. Increased production of CSPGs by reactive astrocytes is responsible for reduced neuronal growth. (A,B) Astrocytes were treated with TGFβ1 for 7 days and conditioned medium was collected and concentrated. After incubation at 37°C for 3 hours with or without cABC, the conditioned medium was immobilized on PLL-coated coverslips, and axonal guidance spot assays were performed. (A) Although axons did not cross the interface between PLL and conditioned medium (arrows, left), many axons cross onto conditioned medium after cABC treatment (right). Scale bar: 25 µm. (B) Quantitative analysis of axonal behavior at the interface. The percentage of axons crossing onto the immobilized conditioned medium was calculated (*,#P<0.05; ANOVA). (C) Inhibition of GAG chain biosynthesis restores neuronal growth. Confluent monolayers of astrocytes were pretreated with TGFβ1, with or without the GAG-chain synthesis inhibitors for 3 days, and neurons were co-cultured for 2 days, followed by the analysis of relative axon length. PNP, p-nitro-phenyl-β-D-xylopyranoside (1 mM); Mu, methyl-umbelliferyl β-D-xyloside (1 mM); SC, sodium chlorate (20 mM) (*P<0.01 compared with TGFβ1-treated astrocytes; ANOVA). Data are expressed as the mean ± s.d.
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