Oxidative stress-induced S100B protein expression from placenta and amnion might affect soluble Endoglin release from endothelial cells.pdf
Author preprint (930.4 kB)
This is an electronic version (Author’s preprint) of an article published in Molecular Human Reproduction;2010 Mar;16(3):188-99;The original published version is available at:http://molehr.oxfordjournals.org/cgi/reprint/16/3/188
[en] Oxidative stress with elevated intracellular Ca(2+) concentration as well as endothelial dysfunction is a component of pre-eclampsia. Our aim was to investigate the oxidative stress-dependent expression of Endoglin and Ca(2+)-binding S100B protein from villous and amniotic tissue cultures, and to assess sEng expression from S100B protein-stimulated endothelial cells. We initially examined Endoglin and Hydroxy-nonenal-(HNE)-modified proteins in the placentas and amnion obtained from women with pre-eclampsia (n = 8), and healthy controls (n = 8) by immunohistochemistry. To examine oxidative stress and the S100B protein effect on sEng expression from endothelial cells, normal villous and amniotic tissue cultures were stimulated by 4-HNE, sodium fluoride and xanthine/xanthine oxidase, whereas human umbilical vein endothelial cell cultures were treated with S100B protein in a dose- and time-dependent manner at 37 degrees C in an environment of 95% air and 5% of CO(2). Culture supernatants were assessed using ELISA. Cell viability was determined using MTS assay. The concentrations of sEng and S100B protein were significantly increased in the villous and amniotic tissue culture supernatants under oxidative stress. S100B protein-stimulated endothelial cells released sEng into conditioned media with a significantly higher expression levels at a concentration of 200 pM-20 nM S100B by 2 h, whereas treated with 200 nM of S100B endothelial cells significantly expressed sEng by 12 h and stimulated the cell proliferation by the same period of time. Our findings show that oxidative stress affects sEng and S100B protein expression from villous and amniotic tissues, and picomolar and low nanomolar concentrations of S100B protein significantly up-regulate sEng release from endothelial cells leading to endothelial dysfunction.
Disciplines :
Reproductive medicine (gynecology, andrology, obstetrics)
Author, co-author :
Tskitishvili, Ekaterine ; Université de Liège - ULiège > Département des sciences cliniques > Labo de biologie des tumeurs et du développement > Osaka University Graduate School of Medicine, Department of Obstetrics and Gynecology
Sharentuya, Namuxila; Osaka University Graduate School of Medicine > Department of Obstetrics and Gynecology
Temma-Asano, Kumiko; Osaka University Graduate School of Medicine > Department of Obstetrics and Gynecology
Mimura, Kazuya; Osaka University Graduate School of Medicine > Department of Obstetrics and Gynecology
Kinugasa-Taniguchi, Yukiko; Osaka University Graduate School of Medicine > Department of Obstetrics and Gynecology
Kanagawa, Takeshi; Osaka University Graduate School of Medicine > Department of Obstetrics and Gynecology
Fukuda, Hirotsugu; Osaka University Graduate School of Medicine > Department of Obstetrics and Gynecology
Kimura, Tadashi; Osaka University Graduate School of Medicine > Department of Obstetrics and Gynecology
Tomimatsu, Takuji; Osaka University Graduate School of Medicine > Department of Obstetrics and Gynecology
Shimoya, Koichiro; Kawasaki Medical School > Department of Obstetrics and Gynecology
Language :
English
Title :
Oxidative stress-induced S100B protein from placenta and amnion affects soluble Endoglin release from endothelial cells.
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