The Inhibitory Core of the Myostatin Prodomain: Its Interaction with Both Type I and II Membrane Receptors, and Potential to Treat Muscle Atrophy
Fig 6
p29 restores the reduced myotube formation resulting from LGMD1C-causing mutant caveolin 3 (CAV3P104L).
(A) Wright-Giemsa-stained C2C12 cells expressing LGMD1C-causing Pro104Leu mutant caveolin 3 (CAV3P104L) at 7 days after differentiation with (+) or without (–)1 μM p29 (left). Scale bar, 100 μm. Fusion indices of these cells following addition of 1 μM of p29 were calculated in triplicate as the percentage of the total nuclei in myotubes/mm2 (right). Values are the means ± SD (n = 5). *P < 0.05. (B) (C) Phase-contrast (left) and fluorescence (right) images of MyHC in C2C12 myoblasts expressing the empty vector (mock) or Pro104Leu mutant caveolin 3 at 7 days after differentiation with (+) or without (–) 1 μM p29. Scale bar, 100 μm. (C) Immunoblot analysis of MyHC and β-actin in C2C12 cells expressing the empty vector (mock) or Pro104Leu mutant caveolin 3 (CAV3P104L) at 7 days after differentiation with (+) or without (–) 1 μM p29 (left). Densitometric analysis (right). Values are mean ± SD fold increases compared with untreated C2C12 cells expressing the empty vector (mock) (n = 5). *P < 0.05.