Fig. 6
From: Astrocytes in mouse models of tauopathies acquire early deficits and lose neurosupportive functions
The active components in C57ACM are macromolecules with a MW above 10 kDa. C57N and P301SN cultures were exposed to complete C57ACM and the same ACM fractionated through a filter with a cut off of ≥10 kDa. The fraction ≥10 kDa (which was diluted to the original volume to offset changes due to concentrating the ACM) or ≤10 kDa was added to the neurons for 8 days. Neurons were counted after immunostaining with the neuronal marker β-III-tubulin. *p < 0.05 for comparisons between number of neurons in: NB vs C57ACM; C57ACM vs C57ACM-10 kDa; C57ACM-10 kDa vs C57ACM + 10 kDa; similar significance was found when C57N or P301SN were treated, statistical analyses was done using Tukey’s multiple comparisons test. ANOVA revealed no interaction on genotype and culture condition (ACM) [F (3, 22 = 0.1457; p = 0.9314], no effect for genotype [F (1, 22) = 0.03553; p = 0.8522] but a significant effect of culture type (ACM) [F (3, 22) = 30.6; p = 0.0001]. The data represent a mean of at least three independent experiments. Each experiment consisted of four technical replicates (wells) in which at least three fields were analyzed