Mesenchymal stem cells promote endothelial progenitor cell proliferation by secreting insulin-like growth factor-1

Bone marrow mesenchymal stem cells (MSCs) and endothelial progenitor cells (EPCs) interact with each other. EPCs are able to promote the self-renewal of MSCs as niche cells in murine bone marrow, and MSCs are able to promote EPC proliferation in vitro in a co-culture system. It has previously been r...

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Veröffentlicht in:Molecular medicine reports 2017-08, Vol.16 (2), p.1502-1508
Hauptverfasser: Hou, Jixue, Peng, Xinyu, Wang, Jing, Zhang, Hongwei, Xia, Jie, Ge, Quanhu, Wang, Xiaoyi, Chen, Xueling, Wu, Xiangwei
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Sprache:eng
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Zusammenfassung:Bone marrow mesenchymal stem cells (MSCs) and endothelial progenitor cells (EPCs) interact with each other. EPCs are able to promote the self-renewal of MSCs as niche cells in murine bone marrow, and MSCs are able to promote EPC proliferation in vitro in a co-culture system. It has previously been reported that MSCs can secrete insulin-like growth factor-1 (IGF-1), which serves critical functions in EPC proliferation. However, the mechanism underlying the IGF-1-mediated proliferation of EPCs remains unclear. The aim of the present study was to reveal the molecular mechanisms regulating this process. The effects of IGF-1, which is secreted by MSCs, on EPC proliferation via the PI3K/Akt signaling pathway were examined by MTT assay, reverse transcription-quantitative polymerase chain reaction and western blot analysis. The present study treated EPCs with various concentrations of IGF-1. The results demonstrated that IGF-1 significantly induced the proliferation of cultured EPCs. However, this effect was offset by treatment with the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002. These results indicated that the pro-proliferative effects of IGF-1 are mediated in response to the PI3K/protein kinase B signaling pathway.
ISSN:1791-2997
1791-3004
DOI:10.3892/mmr.2017.6741