Placental glucose transporter (GLUT)-1 is down-regulated in preeclampsia.

Lüscher, Benjamin; Marini, Camilla; Jörger Messerli, Marianne; Huang, Xiao; Hediger, Matthias; Albrecht, Christiane; Baumann, Marc Ulrich; Surbek, Daniel (2017). Placental glucose transporter (GLUT)-1 is down-regulated in preeclampsia. Placenta, 55, pp. 94-99. Elsevier 10.1016/j.placenta.2017.04.023

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INTRODUCTION Transplacental fetal glucose supply is predominantly regulated by glucose transporter-1 (GLUT1). Altered expression and/or function of GLUT1 may affect the intrauterine environment, which could compromise fetal development and may contribute to fetal programming. To date it is unknown whether placental GLUT1 is affected by preeclampsia, which is often associated with intrauterine growth restriction (IUGR). We addressed the hypothesis that preeclampsia leads to decreased expression and function of placental GLUT1. METHODS Placentae were obtained following normal pregnancy and from pregnancies affected by preeclampsia. Washed villous tissue fragments were used to prepare syncytial microvillous (MVM) and basal plasma membranes (BM) microvesicles. GLUT1 protein and mRNA expression was assessed by western blot analysis and qPCR using Fast SYBR Green. A radio-labeled glucose up-take assay using placenta-derived syncytial microvesicles was used to analyze GLUT1 function. RESULTS GLUT1 protein expression was significantly down-regulated in (apical) MVM of the syncytiotrophoblast in preeclampsia (n = 6) compared to controls (n = 6) (0.40 ± 0.04 versus 1.00 ± 0.06, arbitrary units, P < 0.001, Student's t-test), while GLUT1 mRNA expression did not show a significant difference. In addition, the functional assay in syncytial microvesicles showed a significantly decreased glucose transport activity in preeclampsia (61.78 ± 6.48%, P < 0.05) compared to controls. BM GLUT1 protein expression was unchanged and glucose up-take into BM microvesicles showed no differences between the preeclampsia and control groups. DISCUSSION Our study shows for the first time that in preeclampsia placental GLUT1 expression and function are down-regulated at the apical plasma membrane of the syncytiotrophoblast. Further studies are needed to assess whether these changes occur also in vivo and contribute to the development of IUGR in preeclampsia.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Gynaecology, Paediatrics and Endocrinology (DFKE) > Clinic of Gynaecology
04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR) > Unit Childrens Hospital > Forschungsgruppe Pränatale Medizin
04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Biochemistry and Molecular Medicine

UniBE Contributor:

Lüscher, Benjamin; Marini, Camilla; Jörger Messerli, Marianne; Huang, Xiao; Hediger, Matthias; Albrecht, Christiane; Baumann, Marc Ulrich and Surbek, Daniel

Subjects:

600 Technology > 610 Medicine & health
500 Science > 570 Life sciences; biology

ISSN:

0143-4004

Publisher:

Elsevier

Language:

English

Submitter:

Kevin Marc Rupp

Date Deposited:

20 Nov 2017 17:32

Last Modified:

02 Feb 2018 13:23

Publisher DOI:

10.1016/j.placenta.2017.04.023

PubMed ID:

28623979

Uncontrolled Keywords:

GLUT1 Glucose transport Placenta Preeclampsia Syncytiotrophoblast

BORIS DOI:

10.7892/boris.106124

URI:

https://boris.unibe.ch/id/eprint/106124

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