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Melatonin inhibits IL‐1β‐induced monolayer permeability of human umbilical vein endothelial cells via Rac activation
Author(s) -
Yuan Xiaochen,
Li Bingwei,
Li Hongwei,
Xiu Ruijuan
Publication year - 2011
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1111/j.1600-079x.2011.00882.x
Subject(s) - umbilical vein , melatonin , endocrinology , chemistry , medicine , biology , microbiology and biotechnology , in vitro , biochemistry
Melatonin is a key factor in the coordination of circadian rhythms and seasonal reproduction. Melatonin and its metabolites directly scavenge free radicals, increase the expression of antioxidant enzymes, and play a role in the anti‐inflammatory phase of defense responses. At present, there are no direct data available as to melatonin’s possible influence on endothelial cell monolayer permeability, which is a major biological process responsible for vascular diseases. The aim of this study was to investigate the effect of melatonin on IL‐1β‐induced human umbilical vein endothelial cells (HUVECs) monolayer permeability and then to test the involvement of small GTPase Rac in the melatonin‐induced endothelial barrier‐protective effects as well as cell contact reorganization. It was found that IL‐1β treatment increased the permeability of HUVECs monolayer, disrupted adherens junctions, and down‐regulated the expression of VE‐cadherin which is the main functional protein of adherens junctions. Melatonin, however, decreased dextran permeability and increased intercellular adherens junction areas reflecting an endothelial cell barrier‐protective response. Furthermore, melatonin dramatically improved IL‐1β‐induced Rac inactivation. Our results show that the barrier‐protective effects of melatonin on endothelial cells are mediated by Rac activation and leads to enhancement of adherens junctions.