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Fig. 8 | Acta Neuropathologica Communications

Fig. 8

From: Endogenous TDP-43 mislocalization in a novel knock-in mouse model reveals DNA repair impairment, inflammation, and neuronal senescence

Fig. 8

Tdp-43∆NLS mice exhibit neuronal senescence phenotype in the CNS and hind-limb muscle. (A-B) Representative IF images with fluorescence-based (β-Gal) senescence staining in the cortex of sham and MN-Tdp-43∆NLS mice (N = 6/group). Nuclei were counterstained with DAPI. Scale bar = 10 µm (A). (B) Quantitation of percent of β-Gal positive senescent cells using paired t-test. ****, P < 0.0001. (C-D) IF images of hind-limb soleus muscle tissues stained with anti-Actin (Alexa-Fluor 647) and fluorescent β-Gal (488 nm) from sham and MN-Tdp-43∆NLS mice. The white arrow indicates defective actin polymerization in the soleus muscle of MN-Tdp-43∆NLS mice. Nuclei were counterstained with DAPI. Scale bars = 20 µm and 10 µm (inset images) (C). (D) Quantitation of percent of β-Gal positive senescent cells using paired t-test. ****, P < 0.0001. (E) Quantitation of relative mRNA levels (fold change) of senescence-associated markers Edn1, p21, and Ankrd1 in cortical tissues of sham and MN-Tdp-43∆NLS mice (N = 6/group). Gapdh served as the internal control. Data are expressed as mean ± SEM and analyzed by multiple paired t-tests. *, P < 0.05

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