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. 2013 Oct 28;203(2):345–357. doi: 10.1083/jcb.201211134

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© 2013 Winbanks et al.

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Figure 3. — Endogenous BMP signaling is altered in models of skeletal muscle growth and wasting. (a) TA muscles were collected from neonatal and young adult mice and the phosphorylation of Smad1/5 was determined by Western blotting (*, P < 0.001 vs. control). n = 3 per time point. (b) Rats subjected to intensive care immobilization (n = 3–6 per treatment) displayed muscle atrophy with increased phosphorylation of pSmad1/5 (*, P = 0.01 vs. control muscles; +, P = 0.002 vs. control muscles; #, P < 0.001 vs. control muscles). (c) Smad1/5^S463/465 phosphorylation was assessed in mice (n = 5 per treatment) with a SOD1^G93A mutation that displays symptoms akin to amyotrophic lateral sclerosis patients. At a time point before the onset of muscle atrophy (60 d; *, P = 0.001 vs. control) and at a point of advanced pathology (90 d; #, P < 0.001 vs. control) Smad1/5 phosphorylation was increased. (d) Smad1/5^S463/465 phosphorylation was assessed by Western blot 3 d (n = 5 per treatment; *, P = 0.007 vs. control), 7 d (n = 6 per treatment; *, P = 0.002 vs. control), and 14 d (n = 5–6 per treatment; *, P = 0.002 vs. control) after excision of a portion of the peroneal nerve supplying the TA muscle in wild-type mice. (e–g) mRNA expression of GDF6 (BMP13), GDF5 (BMP14), BMPR1A, BMPR1B, Smad6, and Noggin was assessed by RT-PCR (n = 4–6 per treatment; see specific time points for p-values). Gene expression was analyzed using the ΔΔCT method of analysis and expression was normalized to 18S. Data are presented as means ± SEM.