Nicotine restores endothelial dysfunction caused by excess sFlt1 and sEng in an in vitro model of preeclamptic vascular endothelium: a possible therapeutic role of nicotinic acetylcholine receptor (nAChR) agonists for preeclampsia.
Nicotine restores endothelial dysfunction caused by excess sFlt1 and sEng in an in vivo model of preeclamptic vascular endothelium.pdf
Author postprint (394.63 kB)
This is an electronic version (Author’s postprint) of an article published in American Journal of Obstetrics and Gynecology; 2010 May;202(5):464.e1-6. The original published version is available at: http://www.ajog.org/article/S0002-9378(10)00067-0/pdf
[en] OBJECTIVE: In this study we tested the hypothesis that nicotine restores proangiogenic functions to endothelial cells pretreated with soluble fms-like tyrosine kinase 1 and/or soluble endoglin. STUDY DESIGN: Wound healing assay and tube formation assay were performed using human umbilical vein endothelial cells treated with nicotine (10(-9) to 10(-6) M), and with various combinations of soluble fms-like tyrosine kinase 1 (100 ng/mL), soluble endoglin (100 ng/mL), and nicotine (10(-7) M). Enzyme-linked immunosorbent assay was performed to measure vascular endothelial growth factor, placental growth factor, and transforming growth factor-beta1 concentrations in the conditioned media treated with nicotine (10(-9) to 10(-6) M). RESULTS: Nicotine significantly facilitated endothelial migration and tube formation. By contrast, soluble fms-like tyrosine kinase 1 and/or soluble endoglin suppressed these endothelial functions. Nicotine restored these soluble fms-like tyrosine kinase 1 and/or soluble endoglin-reduced endothelial functions. Placental growth factor, but not transforming growth factor-beta1, production was significantly stimulated by the presence of nicotine. Vascular endothelial growth factor was undetectable. CONCLUSION: Our results suggest a possible mechanism for the protective effects of cigarette smoking against preeclampsia, thus proposing a therapeutic potential of nicotine or other nicotinic acetylcholine receptor agonists for preeclampsia.
Disciplines :
Reproductive medicine (gynecology, andrology, obstetrics)
Author, co-author :
Mimura, Kazuya; Osaka University Graduate School of Medicine > Department of Obstetrics and Gynecology
Tomimatsu, Takuji; Osaka University Graduate School of Medicine > Department of Obstetrics and Gynecology
Sharentuya, Namuxila; Osaka University Graduate School of Medicine > Department of Obstetrics and Gynecology
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
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
Kimura, Tadashi; Osaka University Graduate School of Medicine > Department of Obstetrics and Gynecology
Language :
English
Title :
Nicotine restores endothelial dysfunction caused by excess sFlt1 and sEng in an in vitro model of preeclamptic vascular endothelium: a possible therapeutic role of nicotinic acetylcholine receptor (nAChR) agonists for preeclampsia.
Publication date :
2010
Journal title :
American Journal of Obstetrics and Gynecology
ISSN :
0002-9378
eISSN :
1097-6868
Publisher :
Mosby, St Louis, United States - Missouri
Volume :
202
Issue :
5
Pages :
464.e1-6
Peer reviewed :
Peer Reviewed verified by ORBi
Commentary :
Copyright (c) 2010 Mosby, Inc. All rights reserved.
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