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Figure 4 | Skeletal Muscle

Figure 4

From: Glypican-1 regulates myoblast response to HGF via Met in a lipid raft-dependent mechanism: effect on migration of skeletal muscle precursor cells

Figure 4

Disruption of lipid rafts diminishes hepatocyte growth factor–dependent signaling. (A) C2C12 myoblasts were serum-starved for 6 hours, and during the last hour the cells were treated with or without methyl-β-cyclodextrin (MβCD) at the indicated concentrations. After two washes with serum-free media, the cells were treated with the indicated concentrations of hepatocyte growth factor (HGF) for 5 minutes. The cell extracts were analyzed by immunoblotting for total HGF receptor (Met), phospho- and total AKT, phosphorylated extracellular signal-regulated kinases 1 and 2 (phospho-ERK1/2) and total ERK1/2, and tubulin was used as a loading control. (B) Quantification from two independent experiments is shown. Statistical significance was assessed using two-way analysis of variance and a Bonferroni multiple-comparisons posttest. *P < 0.05, **P < 0.01, ***P < 0.001. (C ) C2C12 myoblasts treated with or without 10 mM MβCD for 1 hour as described in (A) were lysed and fractionated in sucrose density gradients as described in Figure 3. The distributions of total Met and caveolin 1 (Cav-1) were determined by immunoblot analysis. In (A) and (C), the molecular weight standards are shown at left.

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