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Figure 6 | Skeletal Muscle

Figure 6

From: Post-natal induction of PGC-1α protects against severe muscle dystrophy independently of utrophin

Figure 6

Post-natal expression of peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α ameliorates muscle damage in dystrophin-deficient (mdx) mice. (A) The inducible PGC-1α mouse (Ind_PGC-1α) possess two transgenic genes: the muscle specific tetracycline-dependent activator (MCK-tTA); and PGC-1α coding region under control of the tet-response element promoter (TRE_PGC-1α). Removal of doxycycline (dox) allows tTA to bind the TRE region and increase expression of PGC-1α. Mice were kept off dox for 4 weeks (from 3 to 7 weeks of age) prior to the experiment. (B) Nine-week-old male control (wild-type; WT), inducible PGC-1α muscle-specific transgenic mice (WT/Ind_PGC-1α), mdx, and inducible PGC-1α muscle-specific transgenic mice in an mdx background (mdx/Ind_PGC-1α) were sacked and quantitative PCR performed on mRNA from gastrocnemius (n = 5 per group). Bars depict relative mRNA expression. (C) Seven-week-old WT, WT/Ind_PGC-1α, mdx and mdx/Ind_PGC-1α mice were sacked and blood was drawn. Serum creatine kinase was measured. Bars represent average level of serum creatine kinase. (D) Evans Blue was injected intraperitoneally 16 hours before sacking into 7-week-old old WT, WT/Ind_PGC-1α, mdx and mdx/Ind_PGC-1α mice. Histological sections from gastrocnemius were analyzed by fluorescence microscopy. (E) Histological sections from quadriceps of 7-week-old WT, WT/Ind_PGC-1α, mdx and mdx/Ind_PGC-1α mice were stained with hematoxylin and eosin. The number of nuclei found in the center of the cell as opposed to on the periphery was counted. Representative images shown (left) with small black arrows indicating centralized nuclei. Bars (right) depict percentage of nuclei counted which were centralized (n = 5). Error bars represent SEM. *P < 0.05. AChR, acetylcholine receptor; NMJ, neuromuscular junction; Ox-phos, oxidative phosphorylation.

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