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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Rab32 connects ER stress to mitochondrial defects in multiple sclerosis

Fig. 2

Rab32 localization in active MS lesions. a–f Immunofluorescence stainings of patient brain tissue from secondary progressive MS showing Rab32 (a, d), neurofilament (b), merged Rab32/neurofilament, including DAPI (c), CHOP (e) and merged Rab32/CHOP, including DAPI (f). Enlarged areas in a–f are shown below (A’–F’). Active chronic lesion, lesion border, and NAWM were identified using H&E and LFB stain of adjacent sections as described in Fig. 1a –c. g–l Representative images from a 12-patient, 9-control study examining expression of RAB32 in 10 μm sections, containing an acute lesion of an MS patient (referring to tissue phenotype (g–i)) and white matter from control subjects (j–l). g Low power image (×100 mag) of clumps of macrophages ingesting myelin stained with oil red-O within the active border of an acute lesion (fresh frozen tissue) surrounded by gray matter and normal-appearing white matter (NAWM) demarked by dotted line. h RAB32 immunostained with DAB nickel chloride localized within the cell bodies of microglial cells at low magnification (×100 mag) and i at higher magnification (×400). j Weak RAB32 expression in the blood vessel and NAWM of a control subject. k Intermediate RAB32 staining in glial cells present in the NAWM of a separate control subject brain section (×100 mag) and l at ×400 magnification. Note the intensity of staining of RAB32 in microglial/macrophage cells in acute lesions of MS patient compared to control subjects. Scale bars in a, b, d, and e = 50 μm and 12.5 μm in c and f

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