1. PDGFRβ triggered by bFGF promotes the proliferation and migration of endothelial progenitor cells via p-ERK signalling.
- Author
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Guo S, Yu L, Cheng Y, Li C, Zhang J, An J, Wang H, Yan B, Zhan T, Cao Y, Zheng H, and Li Z
- Subjects
- Animals, Cell Movement, Cells, Cultured, Endothelial Cells metabolism, Extracellular Signal-Regulated MAP Kinases metabolism, Phosphorylation, RNA, Messenger genetics, Rats, Receptor, Platelet-Derived Growth Factor beta genetics, Signal Transduction, Stem Cells metabolism, Cell Proliferation, Endothelial Cells cytology, Fibroblast Growth Factor 2 metabolism, MAP Kinase Signaling System, Receptor, Platelet-Derived Growth Factor beta metabolism, Stem Cells cytology
- Abstract
We have examined the effects of bFGF (basic fibroblast growth factor) on p-ERK (phosphorylated extracellular signal-regulated kinase) through PDGFRβ (platelet-derived growth factor receptor β) in the proliferation and migration of EPCs (endothelial progenitor cells). EPC migration was detected using the Transwell system. The expression of PDGFRβ mRNA and protein, total ERK and p-ERK proteins was respectively assessed by real-time PCR and Western blottings. bFGF promote the proliferation and migration of EPCs, the effects of bFGF being implemented by activating ERK signalling through the expression of PDGFRβ, whereas an anti-bFGF antibody and inhibitor of PDGF (platelet-derived growth factor) receptor kinase (AG1296) could respectively decrease the expression of PDGFRβ mRNA and protein and p-ERK protein. Total ERK protein did not change under the same experimental conditions, and an inhibitor of p-ERK (PD98059) inhibited the proliferation and migration of EPCs. The findings strongly suggest that a PDGFRβ/p-ERK signalling pathway triggered by bFGF plays an important role in the proliferation and migration of EPCs.
- Published
- 2012
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