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Role of the bradykinin receptor (B2R) in differentiation, migration, and proliferation of endothelial progenitor cells (EPC)
Author(s) -
Bakdash Nadia,
Wu Yi,
Colman Robert W.
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.116.9
Subject(s) - progenitor cell , bradykinin , chemistry , microbiology and biotechnology , receptor , agonist , medicine , endocrinology , stem cell , biology , biochemistry
As a potent activator of endothelial cells, bradykinin is known to induce vasodilation, vascular permeability, and nitric oxide production. Bradykinin signaling is initiated by binding to the G protein‐coupled receptor B1R and/or B2R. B2R is constitutively expressed in endothelial cells. Endothelial Progenitor Cells (EPCs) are bone‐marrow derived cells that have the potential to differentiate into mature endothelial cells. We now report that EPCs undergo differentiation, migration, and proliferation without addition of exogenous growth factors. Moreover, EPCs stimulated with bradykinin (250 nM) potentiated differentiation (tube formation), migration, and proliferation by 1.4, 1.6, and 1.7‐fold, respectively. Pre‐incubation of the EPCs with HOE‐140 (1 μM or 10 μM), a B2R selective antagonist, reduced differentiation by 70% (p<0.001), modulated migration by 40% (p<0.001), and inhibited proliferation by 20% (p<0.05), indicating that EPCs utilize the BR2 receptor in these three responses. In addition, we demonstrate that EPCs stimulated with the selective B2R peptidomimetic agonist FR190997 (50 nM) enhanced migration. Furthermore, when pre‐incubated with the B2R antagonist, the migration of EPCs was inhibited by 40% (p<0.05). Thus, we conclude that EPCs utilize the B2 receptor for potentiation of migration, differentiation, and proliferation. NIH 2T32HL007777.