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Estradiol (βE) Promotes Adhesion and Mitogenesis in CD34 + Human Progenitor Endothelial Cells (PECs)
Author(s) -
Baruscotti Isabella,
Barchiesi Fedreica,
Jackson Edwin K.,
Gillespie Delbert G.,
Imthurn Bruno,
Dubey Raghvendra K.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.941.12
Subject(s) - adhesion , chemistry , microbiology and biotechnology , cell adhesion , cell growth , agonist , progenitor cell , cyclin d1 , medicine , endocrinology , apoptosis , biology , cell cycle , receptor , stem cell , biochemistry , organic chemistry
Here we investigated whether βE promotes endothelium recovery by promoting PECs adhesion and proliferation. PECs were isolated from blood using CD34 + ‐antibody‐based magnetic separation and placed in culture or used for adhesion studies. For adhesion studies, early PECs, late differentiated PECs or mononuclear cells (MNC) labelled with fluorescent‐dye calcein were layered over monolayers of endothelial cells (ECs) pre‐treated with βE, and the number of adherent cells analyzed by ELISA. βE promoted adhesion of early PECs, but not late differentiated PECs or MNC, to ECs. Increased PECs colony formation and proliferation were observed in cultures of MNC isolated from IVF subjects where βE synthesis was induced. PECs expressed functional ERα and ERβ, and βE induced PECs growth (DNA/cell number) The mitogenic effects of âE were mimicked by PPT (ERα agonist), but not DPN (ERβ agonist), moreover these effects were blocked by ICI (ER antagonist) and MPP (ERα antagonist), βE treatment induced ERK1/2 phosphorylation and upregulated positive growth regulators including cyclin D1, A, B and E and downregulated the negative growth regulator p21. The effects of βE were mimicked by PPT but not DPN, moreover, ICI and MPP blocked the effects, suggesting the effects are ERα mediated. Conclusion βE selectively promotes the adhesion of early CD34 + PECs to ECs and promotes their proliferation via ERα mediated ERK1/2 activation.