Premium
Involvement of NADPH oxidase in serotonin‐induced angiogenesis
Author(s) -
Kim Hyun-Young,
Neupane Ganesh Prasad,
Kim Jung-Ae
Publication year - 2012
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.26.1_supplement.lb770
Subject(s) - apocynin , angiogenesis , nadph oxidase , chemistry , microbiology and biotechnology , pharmacology , biology , reactive oxygen species , cancer research
Serotonin (5‐Hydroxytrytamine, 5‐HT), a gastrointestinal paracrine hormone, has been shown to induce angiogenesis. Reactive oxygen species (ROS) play a role in vascular endothelial growth factor (VEGF)‐induced angiogenesis as a receptor downstream signaling molecule. In vascular endothelium, multi‐subunit NADPH oxidase is the predominant contributor of endothelial superoxide generation. In the present study, we investigated whether NADPH oxidase is involved in serotonin‐induced angiogenesis. Seroton‐ininduced‐ angiogenesis was confirmed by in vivo chick chorioallantoic membrane (CAM) assay. In vitro angiogenesis using human umbilical vein endothelial cells (HUVEC), serotonin enhanced cell migration, invasion and tube formation. Such serotonin‐induced‐angiogenesis was inhibited by cyanopindolol, 5‐HT 1A receptor antagonist, cinanserin, 5‐HT 2A receptor antagonist, and apocynin, NADPH oxidase inhibitor. Serotonin produced ROS, and such ROS was inhibited by apocynin and diphenyl iodonium (DPI), NADPH oxidase inhibitors, but not by allopurinol (Xantine oxidase inhibitor) and anitmycin A (mitochondrial inhibitor). In conclusion, serotonin‐induced angiogenesis is mediated through 5‐HT 1A and 5‐HT 2A receptor, which, in turn, activates NADPH oxidase to generate ROS as a a receptor downstream signaling molecule.