Skip to main content
Fig. 1 | Skeletal Muscle

Fig. 1

From: Absence of physiological Ca2+ transients is an initial trigger for mitochondrial dysfunction in skeletal muscle following denervation

Fig. 1

Denervated muscle fibers show an enhanced mitoflash activity, and CypD is involved in this activity. The representative confocal images of muscle fibers isolated from the FDB muscles with sham (a1–3), denervation (Den) (b1–3), and denervation + CsA treatment (Den + CsA) (c1–3). Panels a1, b1, and c1 show the initial fluorescence images at t = 0 s. Panels a2, b2, and c2 show the peak intensity map of all mitoflashes detected in 100 recorded images. Panels a3, b3, and c3 are the 3D surface plots of (a2, b2, and c2). The quantification analysis of the mitoflashes for three conditions are illustrated in d Total Flash Area/Fiber Area (in 100 sequential images), e FAHM, and F the amplitude (dF/F0) of the mitoflashes. Note that live skeletal muscle fibers respond to the 24-h denervation with dramatically increases of the mitoflash signal in mitochondria, while the CsA treatment restored the Total Flash Area/Fiber Area close to the normal level and significantly reduced the FAHM and signal amplitude (n = 57–64, *p < 0.05). g Immunoblot assay of CypD expression level in both mitochondria (CypD-mito) and cytosol (CypD-cyto) of the skeletal muscle with and without 24-h denervation. h The ratio of CypD in mitochondria over the CypD in cytosol (CypD-mito/CypD-cyto) was quantified. The annotated numbers in parentheses indicate the individual immunoblot assay experiments for denervated skeletal muscle. Note that the 24-h denervation promoted the translocation of CypD from cytosol to mitochondria (n = 5, *p < 0.05)

Back to article page