Muscular atrophy of caveolin-3–deficient mice is rescued by myostatin inhibition
J. Clin. Invest. Yutaka Ohsawa, et al. 116:2924 doi:10.1172/JCI28520 [
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Figure 2Caveolin-3 inhibits intracellular myostatin (MSTN) signaling in vitro. (
A) Immunoblot analysis of total Smad2 (Smad2) and p-Smad2 in cell lysates from COS-7 cells transfected with empty vector (p-CS2+), wild-type caveolin-3 (p-CS2 + wild-type CAV-3), or P104L mutant caveolin-3 (p-CS2 + mutant CAV-3) in the presence or absence of recombinant myostatin (rec. MSTN) (left). Quantification of the fold increase of phosphorylated Smad2 in cell lysates in response to myostatin (right). Data are expressed as mean ± SD (
n = 5). *
P < 0.05. (
B) Myostatin-induced luciferase activity in HEK293 cells cotransfected with a Smad-responsive reporter gene and empty vector, wild-type caveolin-3, or mutant caveolin-3. Data are expressed as mean ± SD (
n = 5). *
P < 0.05. Immunoblot analysis of caveolin-3 in cell lysates is shown in the lower panel.
