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Neuropeptide Y receptor Y 2 is involved in morphogenic modulation of VEGF‐induced coronary vessel formation
Author(s) -
Teplitsky Diana,
Dedkov Eduard I
Publication year - 2011
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.25.1_supplement.684.3
Subject(s) - neuropeptide y receptor , receptor , medicine , neuropeptide , blockade , endocrinology , chemistry , in vitro , vegf receptors , microbiology and biotechnology , biology , biochemistry
This study tested the hypothesis that selective blockade of neuropeptide Y (NPY) receptors Y 1 and/or Y 2 will affect the embryonic formation of coronary vessels induced by VEGF using an in vitro heart explant model. The ventricular apices from the hearts of C57BL/6 mouse embryos (E13) were placed on collagen I gel and cultured for 96 hrs in medium with 10% FBS. For the next 72 hrs the explants were cultured in medium with 1% FBS and treated with the Y receptor selective antagonists (10 nmol/μL) in the presence of NPY (1 nmol/μL) and/or VEGF (50 ng/mL). The explants were stained with Alexa Fluor 594‐labeled GS‐I Isolectine B4 and the total length of endothelial outgrowths (TLO) was quantified using Image‐Pro Plus software. In each explant TLO was normalized by the explant perimeter and finally TLO of experimental explants was expressed as a percentage of TLO in control (VEGF‐treated) explants. The VEGF‐induced formation of endothelial outgrowths was not modified by stimulation of either Y receptor. However, selective blockade of Y 2 receptors, but not of Y 1 receptors, showed significant reduction in formation of VEGF‐induced cord‐like endothelial structures by ~68% (P<0.001). In addition, Y 2 receptor blockade seemed to decrease the number of endothelial cells within the area surrounding the explants. Our data demonstrates that the NPY/Y 2 signaling system plays a modulatory role in VEGF‐induced coronary vessel formation. Grant Funding Source : Internal Award form the NYCOM Office of Research