Reference : Nicotine restores endothelial dysfunction caused by excess sFlt1 and sEng in an in vitro...
Scientific journals : Article
Human health sciences : Reproductive medicine (gynecology, andrology, obstetrics)
http://hdl.handle.net/2268/70072
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.
English
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 - ULg > 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 > > >]
[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.
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