Figure 4: TRAF1 modulates neuronal apoptosis in ischaemic brain.
From: TRAF1 is a critical regulator of cerebral ischaemia–reperfusion injury and neuronal death
(a) Fluorescence staining of cleaved caspase-3 (red) and nuclei (DAPI, blue) in the brains of WT, TRAF1-KO, NTG, and TG2-TRAF1 mice after 24 h of I/R. Scale bar, 100 μm. The inset shows a higher magnification view. Scale bar, 20 μm. The right panel shows the quantification of immunopositive cells (n=3–4, *P<0.05 versus WT, #P<0.05 versus NTG). (b) Quantitation of the indicated mRNA levels (n=4, *P<0.05 versus WT, #P<0.05 versus NTG). (c,d) Immunoanalysis of pro-apoptotic proteins in the brain extracts of WT and TRAF1-KO (c) and TG2-TRAF1 and NTG (d) mice 6 h after sham surgery or I/R. The right panels show the quantification of normalized protein levels (n=6, *P<0.05 versus sham-operated WT (c) or NTG (d); #P<0.05 versus I/R-operated WT (c) or NTG (d)). (e) Immunoanalysis of TRAF1 in neurons infected with the indicated adenoviral vectors (left) and quantification of TRAF1 expression normalized to GAPDH (right) (n=6, *P<0.05 versus Ad-shRNA, #P<0.05 versus Ad-GFP). (f,g) Cell viability (f) and LDH release (g) after adenoviral infection of neurons challenged by OGD for the indicated times (n=6 for each time point, *P<0.05 versus Ad-GFP, #P<0.05 versus Ad-shRNA). The data represent the mean±s.d. Statistical analysis was carried out by unpaired Student’s t-test.
