Fig 1.
Representative coronal sections of infarct area on triphenyltetrazolium chloride (TTC) staining at 24 hr after permanent middle cerebral artery occlusion.
Infarct volume was measured as 22.9 ± 2.9% of the contralateral hemisphere. Scale bar = 5 mm.
Fig 2.
Rotarod treadmill performance. Line graph shows the temporal profile of functional recovery in vehicle-, BMSC-, non-Muse cell-, and Muse cell-treated mice subjected to permanent middle cerebral artery occlusion (pMCAO).
**, ††, ¶¶ P<0.01 vs. vehicle-treated mice. Sec indicates seconds.
Fig 3.
Effects of cell therapy with vehicle, BMSCs, non-Muse cells, and Muse cells on memory impairment at 7 and 35 days after permanent middle cerebral artery occlusion (pMCAO).
Correct choices (A) and errors (B) in the eight-arm radial maze task. **, ††, ¶¶ P<0.01 vs. vehicle-treated mice.
Fig 4.
Low-power photomicrographs of fluorescence immunohistochemistry using anti-human mitochondria antibody in BMSC-, non-Muse cell-, and Muse cell-treated mice at 42 days after transplantation.
A large number of human mitochondria-positive cells are engrafted in the peri-infarct area in Muse cell group. Graph shows number of human mitochondria-positive cells/mm2 in ipsilateral cortex of each group. Scale bars = 500 μm.
Fig 5.
Double immunohistochemistry of GFP-Tuj-1 (A and B), GFP-neuronal nuclear antigen (NeuN; C) and human mitochondria-GFAP (D) in ipsilateral cortex of Muse cell-group (42 days after transplantation).
The white square in panel A represents the location of Panel B. Scale bars = 50 μm.
Fig 6.
Column graph shows the percentages of Tuj1-, NeuN- and GFAP-positive cells in GFP(+) cells in Muse group (42 days after transplantation).