Journal: Neuroscience research

Article Title: The potential mechanism maintaining transactive response DNA binding protein 43 kDa in the mouse stroke model.

doi: 10.1016/j.neures.2025.01.006

Figure Lengend Snippet: Fig. 3. TDP-43 expression changed in parallel with G3BP1 expression. (a) Double immunofluorescence analysis for TDP-43 and G3BP1. Representative results are shown. (b) Quantitative analysis of TDP-43 immunofluorescence analysis by integrated density (IntDen). TDP-43 expression increased significantly in the cortical penumbra area and peaked at 6 h post reperfusion in both 30 min and 60 min tMCAO groups, followed by a decreasing trend in both tMCAO groups. (c) Quantitative analysis of G3BP1 immunofluorescence analysis by IntDen. (d) A scatter diagram of the TDP-43 IntDen and G3BP1 IntDen. G3BP1 expression increased as did TDP-43 expression (ρ= 0.5456, P < 0.0001; Spearman’s correlation coefficient test). (e) Quantitative analysis of TDP-43/G3BP1 double-positive cells. Significant differences were observed between 6 h and 24 h after 60 min tMCAO groups compared with the sham operation group in each visual field. Significant differences were also observed between 6 h and 24 h after 60 min tMCAO groups compared with 30 min tMCAO groups (**, P < 0.01 in 30 min tMCAO group versus sham group; &, &&, &&&&, P < 0.05, P < 0.01, and P < 0.0001 in 60 min tMCAO group versus sham group; $, P < 0.05 in 30 min tMCAO group; §, §§§§, P < 0.05 and P < 0.0001 in 60 min tMCAO group; two-way ANOVA with the Tukey-Kramer multiple comparisons test).

Article Snippet: These were then incubated at 4°C overnight with the following primary antibodies: mouse anti-TDP-43 antibody (1:100, Santa Cruz, sc-376532), rabbit anti-G3BP1 antibody (1:500, Proteintech, 13057–2-AP), and rabbit anti-RAD23B antibody (1:300, Proteintech, 12121–1-AP).

Techniques: Expressing, Immunofluorescence

Journal: Neuroscience research

Article Title: The potential mechanism maintaining transactive response DNA binding protein 43 kDa in the mouse stroke model.

doi: 10.1016/j.neures.2025.01.006

Figure Lengend Snippet: Fig. 5. Total number of positive cells and pixel intensity of proteasomal degradation marker RAD23B were upregulated after tMCAO. (a) Immunohistochemistry for RAD23B at the peri-ischemic lesion. (b) Quantitative analyses of total number of RAD23B-positive cells. (c) Quantitative analyses of RAD23B pixel intensity. Scale bar = 200 μm. (d) Representative double immunofluorescence captures for TDP-43 and RAD23B showed colocalization of TDP-43 and RAD23B at 24 h post reperfusion, either in the 30 min or 60 min tMCAO group. The small panels display a representative double-positive cell. Scale bar = 50 μm. (e) Quantitative analysis of TDP-43/RAD23B double-positive cells per visual field. There were significant differences between 24 h after 30 min tMCAO compared with the sham operation group, and between 1 h, 6 h, 24 h after 60 min tMCAO compared with the sham operation group (** and ***, P < 0.01 and P < 0.001 in 30 min tMCAO group versus sham group; &, &&&, and &&&&, P < 0.05, P < 0.001, and P < 0.0001, respectively, in 60 min tMCAO group versus sham group; # and ##, P < 0.05 and P < 0.01 in 60 min versus 30 min tMCAO group; § and §§, P < 0.05 and P < 0.01 in 60 min tMCAO group; two-way ANOVA with the Tukey-Kramer multiple compari sons test).

Article Snippet: These were then incubated at 4°C overnight with the following primary antibodies: mouse anti-TDP-43 antibody (1:100, Santa Cruz, sc-376532), rabbit anti-G3BP1 antibody (1:500, Proteintech, 13057–2-AP), and rabbit anti-RAD23B antibody (1:300, Proteintech, 12121–1-AP).

Techniques: Marker, Immunohistochemistry, Immunofluorescence