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. 2011 Feb 9;6(2):e14675. doi: 10.1371/journal.pone.0014675

Figure 2. Analysis of Met expression and downstream signalling activation in neonatal cardiomyocytes.

Figure 2

(A) Immunofluorescence of Met receptor (red) and GFP (green) in neonatal (P7) heart samples of control (left panel) and HGF tg mice (middle panel). A negative control of secondary antibody was included (right panel). Bars: 50µm. (B) Western blot of Met (p140Met) protein in control and HGF tg mice at different ages post-birth (P2 n = 6 n = 7, P4 n = 8 n = 6, P7 n = 10 n = 11, P18 n = 9 n = 14). Representative blots are shown below densitometric quantification (normalized on GAPDH loading control, relative to P2 control). Controls vs HGF tg mice: *p<0.05 and †p<0.005 (two-tailed T-test). (C) Densitometric quantification (normalized on tubulin loading control) and representative Western blot of phospho-Erk1,2 (P Erk1,2), phospho-p38 MAPK (P p38) and phospho-Akt (P Akt) in HGF tg (n = 7) relative to control mice (n = 6) at two days post birth (P2). *p<0.05 (two-tailed T-test). (D) Western blot analysis of Met receptor and downstream signalling after treatment of H9c2 cardiomyoblast cell line with 10U/ml of HGF for different lengths of time. Densitometric quantification was normalized against tubulin and plotted as relative to time 0′ of treatment. Each condition was tested 3 times.