Fig. 8: MT densification and fragmentation of Golgi in αMHC-MCM-Fktn-cKO (Fktnflox/flox; αMHC-MCM+/−) myocytes. | Nature Communications

Fig. 8: MT densification and fragmentation of Golgi in αMHC-MCM-Fktn-cKO (Fktnflox/flox; αMHC-MCM+/−) myocytes.

From: Elimination of fukutin reveals cellular and molecular pathomechanisms in muscular dystrophy-associated heart failure

Fig. 8

a Representative immunofluorescence images for MT (green) and GM130 (red) staining. Arrowheads show abnormally distributed GM130 signals. Scale bar, 50 μm (insets, 10 μm). b Electrical stimulation-induced (1 Hz) myocyte shortening (vehicle-intact, n = 101 cells from 5 mice; vehicle-colchicine, n = 40 cells from 4 mice; vehicle-ilimaquinone, n = 20 cells from 3 mice, tamoxifen-intact, n = 29 cells from 3 mice; tamoxifen-colchicine, n = 40 cells from 3 mice). c Representative images of immunoblots. Phosphorylation level of PKD is shown relative to total PKD (n = 6 mice per group). *P < 0.05 vs. vehicle-treated floxed mice; #P < 0.05 between indicated groups based on Tukey–Kramer tests. d Normalized peak amplitudes (vehicle-intact, n = 32 cells from 4 mice; vehicle-colchicine, n = 39 cells from 3 mice; vehicle-ilimaquinone, n = 26 cells from 3 mice, tamoxifen-intact, n = 14 cells from 4 mice; tamoxifen-colchicine, n = 11 cells from 4 mice). e Contractile efficiency (vehicle-intact, n = 8 cells; vehicle-colchicine, n = 6 cells; vehicle-ilimaquinone, n = 6 cells, tamoxifen-intact, n = 5 cells; tamoxifen-colchicine, n = 6 cells from 3 mice per group). #P < 0.05 between indicated groups based on Tukey–Kramer tests (b, d, e).

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