Estrogen induces endothelial progenitor cells proliferation and migration by estrogen receptors and PI3K-dependent pathways.

Abstract:

:Estrogen induces endothelial progenitor cells (EPCs) migration and proliferation, which may serve as a potential target for coronary artery disease, but the mechanisms are unclear. We hypothesized that estrogen receptors (ERs) and phosphatidylinositol 3-kinase (PI3K) signaling pathway, which represent particularly important roles of action for estrogen, may contribute to estrogen-induced EPCs migration and proliferation. Bone marrow mononuclear cells (MNCs) were cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with growth factors as previously described. A total of 87.32+/-5.13% of adherent cells showed uptake of acetylated low-density lipoprotein and lectin binding. Immunostaining and fluorescence activated cell sorting confirmed the endothelial progenitor phenotype. RT-PCR, immunocytochemistry staining and Western blot demonstrated expression of ERs. Exposure to 17beta-estradiol significantly improved EPCs migration and proliferation. Those effects were blocked by pretreatment with the pharmacological PI3K blockers LY294002 (1 h, 10 micromol/L) and ICI-182780 (1 h, 10 micromol/L), a specific estrogen receptor antagonist, which show involvement of estrogen receptors and PI3K pathway. These results suggest that estrogen induces EPCs migration and proliferation via ERs and PI3K pathway which provided a novel insight and treatment strategy of vascular biology.

journal_name

Microvasc Res

journal_title

Microvascular research

authors

Zhao X,Huang L,Yin Y,Fang Y,Zhao J,Chen J

doi

10.1016/j.mvr.2007.02.009

subject

Has Abstract

pub_date

2008-01-01 00:00:00

pages

45-52

issue

1

eissn

0026-2862

issn

1095-9319

pii

S0026-2862(07)00024-6

journal_volume

75

pub_type

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