Figure 7.

Molecular signaling in the regulation of reactive astrocyte hypertrophy. (a) Activities of various signaling proteins in injured cortices of Mlc1-dnEGFR (M) and littermate control mice (T) 3 days post injury were examined by WB. Note the specific reduction of phosphorylated FAK (pFAK) and Src (pSrc), as well as profilin (pProfilin), in the injured cortical tissues from Mlc1-dnEGFR mice in comparison with that from littermate controls. (b) Quantitative analyses of the protein phosphorylation levels revealed by WB. Phosphorylation levels of indicated proteins were normalized by its total protein levels. **P<0.01; *P<0.05; n=3 for each protein, paired t-test. (c) Specific reduction of FAK and Src activities in the reactive astrocytes of Mlc1-dnEGFR mice in comparison with that of littermate controls. Cortical slices from injured Mlc1-dnEGFR and littermate control mice were co-immunostained by mouse antibody against GFAP and rabbit/goat antibodies against the active forms of FAK or Src, respectively. White arrows, representative double positive cells. ‘Δ’ represents the injury sites. (d) Percentage of reactive astrocytes with active FAK or Src according to immunostaining results. Only cells positive for GFAP were analyzed. **P<0.01; *P<0.05; n=4 for each group, paired t-test. (e) Average levels of FAK or Src phosphorylation in individual reactive astrocytes according to immunostaining results. Only cells positive for GFAP were analyzed. *P<0.05; n=4 for each group, paired t-test.