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. 2014 Feb 20;23(14):3706–3715. doi: 10.1093/hmg/ddu079

Figure 2.

Figure 2.

STIM1 overexpression in skeletal muscle gives rise to histological and biochemical features of muscular dystrophy. (A) Representative H&E-stained histological sections from quadriceps and soleus muscle obtained from 6-week-old Wt and STIM1 TG mice. Magnification is ×200. (B) Quantification of myofibers with centrally located nuclei as a maker of regeneration in the diaphragm (three sections/muscle were analyzed), quadriceps (five sections/muscle were analyzed) and soleus (two sections/muscle were analyzed) muscles in Wt and STIM1 TG mice at 6 weeks and 6 months. The total number of mice/muscles analyzed is shown in the bars for the quadriceps. (C) Interstitial fibrosis quantified by metamorph analysis software in Masson's trichrome-stained histological sections of diaphragm (Dia), quadriceps (Quad) and soleus (Sol) obtained from mice sacrificed at the indicated ages. (D) Biochemical analysis of hydroxyproline content for fibrosis in the quadriceps normalized to muscle weight in Wt and STIM1 TG mice. (E) Quantitation of serum creatine kinase (CK) levels in Wt and STIM1 TG mice at 6 weeks and 6 months. (F) Quantitation of calpain activity in Wt and STIM1 TG quadriceps at 6 weeks of age (Relative luciferase activity is shown as part of a calpain assay). (G) NFAT luciferase activity assessed in muscle lysates obtained from Wt and STIM1 TG mice also carrying the NFAT luciferase reporter transgene. *P < 0.05 compared with Wt mice and the number of animals used as shown in the bars of each panel.