Figure 5
Figure 5. p38, p53, JNK, and Akt pathways are influenced by BMSC-derived exosome. 5T33MMvt cells in serum-free medium were treated with or without 40 μg/mL naive (A) or 5T33 (B) BMSC-derived exosomes for indicated times. Expressions of total and phosphorylated insulin-like growth factor 1 receptor β, Erk1/2, p53, JNK, p38, and Akt in MM cells were determined using western blot analysis. 5T33MMvt (C,E) or 5T33MMvv (D,F) cells were treated with 40 μg/mL naive or 5T33 BMSC-derived (NB or 5B) exosomes in serum-free conditions for 24 hours. The total and phosphorylated p53, JNK, p38, and Bim and the expression of Bcl-2, Bax, and caspase-3 were detected using western blot. The analysis of β-actin protein was included as a loading control. The pixel densities of p53, p38, BimEL, and JNK in 5T33MMvt (E) or 5T33MMvv (F) cells after 24 hours of treatment were quantified from 3 independent experiments. The pixel density of phosphorylations of p53, p38, and JNK were normalized to their total proteins. The expression of BimEL was normalized to β-actin, and all these results were presented by histograms. Mean values ± standard deviation for 3 independent experiments are shown. *P < .05; **P < .01; ***P < .001.

p38, p53, JNK, and Akt pathways are influenced by BMSC-derived exosome. 5T33MMvt cells in serum-free medium were treated with or without 40 μg/mL naive (A) or 5T33 (B) BMSC-derived exosomes for indicated times. Expressions of total and phosphorylated insulin-like growth factor 1 receptor β, Erk1/2, p53, JNK, p38, and Akt in MM cells were determined using western blot analysis. 5T33MMvt (C,E) or 5T33MMvv (D,F) cells were treated with 40 μg/mL naive or 5T33 BMSC-derived (NB or 5B) exosomes in serum-free conditions for 24 hours. The total and phosphorylated p53, JNK, p38, and Bim and the expression of Bcl-2, Bax, and caspase-3 were detected using western blot. The analysis of β-actin protein was included as a loading control. The pixel densities of p53, p38, BimEL, and JNK in 5T33MMvt (E) or 5T33MMvv (F) cells after 24 hours of treatment were quantified from 3 independent experiments. The pixel density of phosphorylations of p53, p38, and JNK were normalized to their total proteins. The expression of BimEL was normalized to β-actin, and all these results were presented by histograms. Mean values ± standard deviation for 3 independent experiments are shown. *P < .05; **P < .01; ***P < .001.

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