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Fig. 5 | Skeletal Muscle

Fig. 5

From: Muscle-specific deletion of SOCS3 increases the early inflammatory response but does not affect regeneration after myotoxic injury

Fig. 5

SOCS3 deletion does not alter regeneration or inflammation after myotoxic injury in aged mice. Twenty-four-month-old control (SOCS3fl/fl MCK-Cre) and SOCS3 MKO (SOCS3fl/fl MCK-Cre+) mice were either left uninjured (UN) or received a single 40 μL injection of notexin (10 μg/ml) into the right TA muscle. a Representative hematoxylin and eosin-stained sections of the TA muscle from uninjured or day 7 injured control and SOCS3 MKO mice. Muscle mass relative to body mass (b) and muscle fiber size (c) was determined at day 7 post-notexin injury. d Western immunoblotting for phosphorylated and total STAT3 protein levels was performed on protein extracted from the remaining OCT embedded muscles following tissue sectioning. Representative immunoblots for phosphorylated (top) and total (bottom) STAT3 protein levels are shown. Band intensity was quantified using ImageQuant software (Bio-Rad Laboratories), and the ratio of phosphorylated/total STAT3 protein levels was determined. Bands used for quantification are indicated by arrows. qRT-PCR using primers to detect Socs3 (e), IL-6 (f), TNF-α (g), IFN-γ (h), F4/80 (i), CD68 (j), Pax7 (k), MyoD (l), or Myogenin (m) was performed on RNA extracted from snap frozen muscles following dissection. Data are expressed as mean ± SEM. Statistical analysis was performed using an unpaired two-tailed Student’s t test (n = 7–8 mice/time-point/genotype) except for analysis of muscle fiber size (c) which was analyzed with a two-way ANOVA and Fisher’s LSD post hoc multiple comparisons test to determine the effect of genotype and injury (n = 4–8 mice/time-point/genotype). Scale bar = 100 μm

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