Fig. 1: CLU is upregulated by astrocytes in MS as well as murine demyelinating lesions. | Nature Communications

Fig. 1: CLU is upregulated by astrocytes in MS as well as murine demyelinating lesions.

From: Astrocyte-derived clusterin disrupts glial physiology to obstruct remyelination in mouse models of demyelinating diseases

Fig. 1

A, B Representative micrographs depicting immunohistochemical staining of CLU and GFAP within the white matter lesions of MS and NMS patients (n = 1 participant/group, p < 0.0001). C, D Immunohistochemical staining revealing elevated CLU levels in the astrocyte within the spinal cord of EAE (n = 3 mice/group, p = 0.0001). E, F Western blot analysis demonstrates a progressive increase in CLU levels correlated with disease severity in the spinal cord of EAE mice (n = 3 mice/group, E1 vs. Ctrl p = 0.4528; E2 vs. Ctrl p < 0.0001; E3 vs. Ctrl p < 0.0001; E4 vs. Ctrl p = 0.0001). G, H Increased CLU levels are observed in LPC-induced demyelinated foci (n > 5 mice/group, Dpi 5 vs. dapi 0 p < 0.0001, Dpi 10 vs. dapi 0 p < 0.0001, Dpi 20 vs. dapi 0 p < 0.0001). I–L In cuprizone-induced demyelinated foci, CLU levels remain unchanged, as evidenced by immunohistochemical staining (n = 3 mice/group, p = 0.6358) and western blot (n = 4 mice/group, p = 0.9852). For immunofluorescence pictures: Scale bar: 50 μm. Statistical analysis was performed using unpaired two-tailed Student’s t-tests, mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001. ns. = p not significant. NMS non-multiple sclerosis, MS multiple sclerosis, Ctrl control, EAE experimental autoimmune encephalomyelitis, E clinical score for EAE, LPC lysolecithin.

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