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过表达 PDGFR-β 通过 PI3K/Akt 信号通路促进 PDGF 诱导的 EPCs 的增殖、迁移和血管生成。

Over-expression of PDGFR-β promotes PDGF-induced proliferation, migration, and angiogenesis of EPCs through PI3K/Akt signaling pathway.

机构信息

Institute of Cardiovascular Science Xinqiao Hospital, Third Military Medical University, Shapingba District, Chongqing, People's Republic of China.

出版信息

PLoS One. 2012;7(2):e30503. doi: 10.1371/journal.pone.0030503. Epub 2012 Feb 15.

DOI:10.1371/journal.pone.0030503
PMID:22355314
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3280261/
Abstract

The proliferation, migration, and angiogenesis of endothelial progenitor cells (EPCs) play critical roles in postnatal neovascularization and re-endothelialization following vascular injury. Here we evaluated whether the over-expression of platelet-derived growth factor receptor-β (PDGFR-β) can enhance the PDGF-BB-stimulated biological functions of EPCs through the PDGFR-β/phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. We first confirmed the expression of endogenous PDGFR-β and its plasma membrane localization in spleen-derived EPCs. We then demonstrated that the PDGFR-β over-expression in EPCs enhanced the PDGF-BB-induced proliferation, migration, and angiogenesis of EPCs. Using AG1295 (a PDGFR kinase inhibitor), LY294002 (a PI3K inhibitor), and sc-221226 (an Akt inhibitor), we further showed that the PI3K/Akt signaling pathway participates in the PDGF-BB-induced proliferation, migration, and angiogenesis of EPCs. In addition, the PI3K/Akt signaling pathway is required for PDGFR-β over-expression to enhance these PDGF-BB-induced phenotypes.

摘要

内皮祖细胞（EPCs）的增殖、迁移和血管生成在血管损伤后的新生血管生成和再内皮化中起着关键作用。在这里，我们评估了过表达血小板衍生生长因子受体-β（PDGFR-β）是否可以通过 PDGFR-β/磷酸肌醇 3-激酶（PI3K）/Akt 信号通路增强 PDGF-BB 刺激的 EPC 生物学功能。我们首先证实了内源性 PDGFR-β及其在脾源性 EPC 中的质膜定位的表达。然后，我们证明了 EPC 中 PDGFR-β的过表达增强了 PDGF-BB 诱导的 EPC 增殖、迁移和血管生成。使用 AG1295（PDGFR 激酶抑制剂）、LY294002（PI3K 抑制剂）和 sc-221226（Akt 抑制剂），我们进一步表明 PI3K/Akt 信号通路参与了 PDGF-BB 诱导的 EPC 增殖、迁移和血管生成。此外，PI3K/Akt 信号通路是 PDGFR-β过表达增强这些 PDGF-BB 诱导表型所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/e1926d8dcd4d/pone.0030503.g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/dad40cd5d56d/pone.0030503.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/2ba9cd168043/pone.0030503.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/4fdfa5bedda5/pone.0030503.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/d71b4c9284c3/pone.0030503.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/04e4fec9b281/pone.0030503.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/eb0125b29e58/pone.0030503.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/f4894f51d6be/pone.0030503.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/aea83ac453e9/pone.0030503.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/b706fde553b4/pone.0030503.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/74f2b09cfefc/pone.0030503.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/e1926d8dcd4d/pone.0030503.g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/dad40cd5d56d/pone.0030503.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/2ba9cd168043/pone.0030503.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/4fdfa5bedda5/pone.0030503.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/d71b4c9284c3/pone.0030503.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/04e4fec9b281/pone.0030503.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/eb0125b29e58/pone.0030503.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/f4894f51d6be/pone.0030503.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/aea83ac453e9/pone.0030503.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/b706fde553b4/pone.0030503.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/74f2b09cfefc/pone.0030503.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8621/3280261/e1926d8dcd4d/pone.0030503.g011.jpg

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本文引用的文献

[1]
Platelet-Derived Growth Factor (PDGF)/PDGF Receptors (PDGFR) Axis as Target for Antitumor and Antiangiogenic Therapy.

Pharmaceuticals (Basel). 2010-3-11

[2]
Endothelial progenitor cells induce a phenotype shift in differentiated endothelial cells towards PDGF/PDGFRβ axis-mediated angiogenesis.

PLoS One. 2010-11-24

[3]
bFGF and PDGF-BB have a synergistic effect on the proliferation, migration and VEGF release of endothelial progenitor cells.

Cell Biol Int. 2011-5

[4]
Intake of red wine increases the number and functional capacity of circulating endothelial progenitor cells by enhancing nitric oxide bioavailability.

Arterioscler Thromb Vasc Biol. 2010-1-21

[5]
Phosphoinositide 3-kinase is a novel target of piceatannol for inhibiting PDGF-BB-induced proliferation and migration in human aortic smooth muscle cells.

Cardiovasc Res. 2009-11-3

[6]
LRP1 regulates architecture of the vascular wall by controlling PDGFRbeta-dependent phosphatidylinositol 3-kinase activation.

PLoS One. 2009-9-9

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Platelet-derived growth factor expression correlates with tumor grade and proliferative activity in human oligodendrogliomas.

Surg Neurol. 2009-7

[8]
Dissociation of phenotypic and functional endothelial progenitor cells in patients undergoing percutaneous coronary intervention.

Heart. 2009-12

[9]
Endothelial progenitor cells control the angiogenic switch in mouse lung metastasis.

Science. 2008-1-11

[10]
Id1 restrains p21 expression to control endothelial progenitor cell formation.

PLoS One. 2007-12-19

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