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Role of β 3 ‐Adrenergic Receptors in Rat Aortic Endothelial Cell Function
Author(s) -
Zahriya Yusuf,
Chang Yingzi
Publication year - 2021
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.2021.35.s1.02915
Subject(s) - endothelial stem cell , cell growth , basic fibroblast growth factor , microbiology and biotechnology , restenosis , cell , vascular endothelial growth factor b , endothelium , receptor , chemistry , biology , medicine , vascular endothelial growth factor , growth factor , vascular endothelial growth factor a , cancer research , biochemistry , in vitro , stent , vegf receptors
Long‐term success of percutaneous trans‐luminal coronary angioplasty (PTCA) is limited by the frequent occurrence of restenosis, resulted from vascular smooth muscle cell (VSMC) proliferation and migration due to the procedure‐induced endothelial damage. Speeding the healing of the endothelial layer has been considered as one of the major approaches to reduce the risk of restenosis. Basic fibroblast growth factor (bFGF), a major growth factor released after injury, regulates endothelial cell proliferation and migration and promotes endothelial layer healing. Our previous results revealed that β 3 ‐adrenergic receptor (β 3 ‐ARs) expression is upregulated in newly formed intima in injured blood vessels and activation of β 3 ‐ARs enhanced bFGF‐induced VSMC proliferation and migration. However, the role of β 3 ‐ARs in endothelial function, specifically in injured arteries, is uncertain. The purpose of this study is to determine if activation of endothelial cell β 3 ‐ARs potentiates bFGF‐induced endothelial cell proliferation and/or migration by using rat aortic endothelial cells. Cell proliferation was determined by measuring viable cell numbers using Resazurin. Cell migration will be quantified by a monolayer wound healing assay in the presence of a cell proliferation inhibitor, hydroxyurea. A dose‐dependent inhibition of cell proliferation was performed to optimize the concentration of hydroxyurea in cell migration experiments. Our results revealed that pretreatment of endothelial cells with a selective β 3 ‐AR agonist, CL316,243, enhanced bFGF‐induced vascular endothelial cell proliferation. We also found that 5μM of hydroxyurea completely inhibited cell proliferation induced by growth factors. In conclusion, our data suggest that activation of β 3 ‐ARs may speed the healing of endothelial layer by promoting cell proliferation and that including 5μM of hydroxyurea in cell migration experiments will allow us to measure the cell motility accurately and ensure that proliferation does not take place.