Fig. 2From: Rab32 connects ER stress to mitochondrial defects in multiple sclerosisRab32 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 Back to article page