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IKVAV regulates ERK1/2 and Akt signalling pathways in BMMSC population growth and proliferation.

Li B, Qiu T, Zhang P, Wang X, Yin Y, Li S - Cell Prolif. (2014)

Bottom Line: IKVAV peptides were synthesized by the solid-phase method.Meanwhile, phosphorylation levels of ERK1/2 and Akt were partially blocked by ERK1/2 inhibitor (PD98059) and Akt inhibitor (wortmannin), respectively.This study is the first to reveal an enhancement effect of IKVAV peptide on BMMSC at the signal transduction level, and the outcome could provide experimental evidence for application of IKVAV-grafted scaffolds in the field of BMMSC-based tissue engineering.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Advanced Technology for Materials Synthesis and Processing, and Biomaterials Science and Engineering Research Center, Wuhan University of Technology, Wuhan, 430070, China.

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Inhibition evaluation of IKVAV-induced phosphorylation levels of ERK1/2 and Akt by inhibitors of ERK1/2 and Akt signaling pathways in BMMSCs. BMMSCs were treated with 0.5 mmIKVAV after pretreatment of PD98059 (10 μm) or wortmannin (100 nm). Cell extracts were prepared at the end of 24 h co-culture, then p-ERK1/2, p-Akt and total ERK, Akt were determined by western blot analysis. Experiments were performed at least in triplicate (*P < 0.05).
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fig05: Inhibition evaluation of IKVAV-induced phosphorylation levels of ERK1/2 and Akt by inhibitors of ERK1/2 and Akt signaling pathways in BMMSCs. BMMSCs were treated with 0.5 mmIKVAV after pretreatment of PD98059 (10 μm) or wortmannin (100 nm). Cell extracts were prepared at the end of 24 h co-culture, then p-ERK1/2, p-Akt and total ERK, Akt were determined by western blot analysis. Experiments were performed at least in triplicate (*P < 0.05).

Mentions: To determine roles of ERK1/2 and Akt signalling pathways activated by IKVAV treatment, MAPK/ERK pathway inhibitor PD98059 and PI3K/Akt pathway inhibitor wortmannin were utilized 58,59. An clear reduction in p-Akt and p-ERK expression was observed after pre-treatment with wortmannin and PD98059 according to western blot analysis. As shown in Fig.5, IKVAV-induced p-ERK1/2 activation was reduced by 23.86% in cells pre-treated with PD98059 at 10 μm compared to the untreated group (Fig.5a). While IKVAV-induced p-Akt activation was reduced by 17.61% in BMMSCs pre-treated with wortmannin at 100 nm compared to the untreated group (Fig.5b). These results indicate that treating BMMSC with 10 μm PD98059 and 100 nm wortmannin effectively blocked the enhanced proliferation of IKVAV-induced BMMSCs.


IKVAV regulates ERK1/2 and Akt signalling pathways in BMMSC population growth and proliferation.

Li B, Qiu T, Zhang P, Wang X, Yin Y, Li S - Cell Prolif. (2014)

Inhibition evaluation of IKVAV-induced phosphorylation levels of ERK1/2 and Akt by inhibitors of ERK1/2 and Akt signaling pathways in BMMSCs. BMMSCs were treated with 0.5 mmIKVAV after pretreatment of PD98059 (10 μm) or wortmannin (100 nm). Cell extracts were prepared at the end of 24 h co-culture, then p-ERK1/2, p-Akt and total ERK, Akt were determined by western blot analysis. Experiments were performed at least in triplicate (*P < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4232901&req=5

fig05: Inhibition evaluation of IKVAV-induced phosphorylation levels of ERK1/2 and Akt by inhibitors of ERK1/2 and Akt signaling pathways in BMMSCs. BMMSCs were treated with 0.5 mmIKVAV after pretreatment of PD98059 (10 μm) or wortmannin (100 nm). Cell extracts were prepared at the end of 24 h co-culture, then p-ERK1/2, p-Akt and total ERK, Akt were determined by western blot analysis. Experiments were performed at least in triplicate (*P < 0.05).
Mentions: To determine roles of ERK1/2 and Akt signalling pathways activated by IKVAV treatment, MAPK/ERK pathway inhibitor PD98059 and PI3K/Akt pathway inhibitor wortmannin were utilized 58,59. An clear reduction in p-Akt and p-ERK expression was observed after pre-treatment with wortmannin and PD98059 according to western blot analysis. As shown in Fig.5, IKVAV-induced p-ERK1/2 activation was reduced by 23.86% in cells pre-treated with PD98059 at 10 μm compared to the untreated group (Fig.5a). While IKVAV-induced p-Akt activation was reduced by 17.61% in BMMSCs pre-treated with wortmannin at 100 nm compared to the untreated group (Fig.5b). These results indicate that treating BMMSC with 10 μm PD98059 and 100 nm wortmannin effectively blocked the enhanced proliferation of IKVAV-induced BMMSCs.

Bottom Line: IKVAV peptides were synthesized by the solid-phase method.Meanwhile, phosphorylation levels of ERK1/2 and Akt were partially blocked by ERK1/2 inhibitor (PD98059) and Akt inhibitor (wortmannin), respectively.This study is the first to reveal an enhancement effect of IKVAV peptide on BMMSC at the signal transduction level, and the outcome could provide experimental evidence for application of IKVAV-grafted scaffolds in the field of BMMSC-based tissue engineering.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Advanced Technology for Materials Synthesis and Processing, and Biomaterials Science and Engineering Research Center, Wuhan University of Technology, Wuhan, 430070, China.

Show MeSH
Related in: MedlinePlus