Fig. 4: SERCA2a is degraded by lysosomes in TMAO-induced cardiomyocyte hypertrophy.

a, b Western blot analysis of SERCA2a and quantification in H9c2 cells treated with TMAO(1 mM) for 24 h, followed by treatment with MG132 (250, 500, 1000 nM) for 24 h, n = 3. The proteasomal substrate MCL1 serves as a control showing the effects of MG132. c, d Western blot analysis of SERCA2a and quantification in H9c2 cells treated with TMAO (1 mM) for 24 h, followed by treatment with BafA1(5, 10, 20 nM) for 24 h, n = 3. e, f Western blot analysis of SERCA2a and quantification in H9c2 cells pretreated with CQ (10 μM) for 1 h and followed by treatment with TMAO (1 mM) for another 48 h, n = 3. g Representative images of immunofluorescence detection of LAMP1 (red) and SERCA2a (green) in H9c2 cells treated with TMAO (1 mM) for 24 h, followed by treatment with BafA1(10 nM) for 24 h. Statistical analyse was performed using the One-way ANOVA with Tukey’s multiple comparisons test. Error bars represent S.E.M.