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. Author manuscript; available in PMC: 2018 Aug 1.
Published in final edited form as: Kidney Int. 2017 May 12;92(2):336–348. doi: 10.1016/j.kint.2017.02.031

Figure 5. Forced expression of SCP4 in muscle results in myofiber atrophy in mice.

Figure 5

a: TA muscles of normal C57B6J mice were transfected with GFP control (GFP) and SCP4-GFP plasmids using electroporation. After 2 weeks, the total nuclear SCP4 (endogenous SCP4 plus SCP4-GFP) was assessed using immunoblots (n=5, **p<0.01); cryosections (6 μm) were immunostained with anti-dystrophin antibody to outline myofibers (red fluorescence). Scale bars: 50 μm.

b: The distribution of myofiber sizes in TA muscles transfected with SCP4-GFP was shifted leftward compared with the result in TA muscles electroporated with CTL-GFP. Data were obtained from 5 animals in each group.

c: Overexpression of SCP4 in TA muscles resulted in a decrease in p-FoxO1 and p-FoxO3a. A statistical analysis of immunoblots was shown on the right (mean±SEM, n = 5/group, **p<0.01,

d: The mRNA level of Myostatin, Atrogin-1, MuRF1 and MUSA1 were examined using RT-PCR in in TA muscles expressed GFP-CTL or GFP-SCP4 (mean±SEM, n = 5/group, **p < 0.01, *p<0.05)