Lüscher, Benjamin; Fine, Michael; Marini, Camilla; Clemençon, Benjamin; Albrecht, Christiane; Hediger, Matthias; Surbek, Daniel; Baumann, Marc Ulrich (September 2014). PLACENTAL URIC ACID TRANSPORTER GLUT9 IS MODULATED BY FREE IODINE. Placenta, 35, A97-A97. Elsevier
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PLACENTAL URIC ACID TRANSPORTER GLUT9 IS MODULATED BY FREE
IODINE
Objectives: Materno-fetal transplacental transport is crucial for the fetal
well-being. The altered expression of placental transport proteins under
specific pathophysiological conditions may affect the intrauterine environment.
Pre-eclampsia is often associated with high maternal uric acid
serum levels. The regulation of the placental uric transport system and its
transporter glucose transporter (GLUT)-9 are not fully understood yet. The
aim of this study was to investigate the placental urate transport and to
characterize its transporter GLUT9.
Methods: In this study we used a transepithelial transport (Transwell®)
model to assess uric acid transport activity. Electrophysiological techniques
and radioactive ligand up-take assays were used to measure
transport activity of GLUT9 expressed in Xenopus oocytes.
Results: In the Transwell/model uric acid is transported across the BeWo
choriocarcinoma cell monolayer with 530 pmol/min at the linear stage. We
could successfully over-express GLUT9 using the Xenopus laevis oocytes
expression system. Chloride modulates the urate transport system: interestingly
replacing chloride with iodine resulted in a complete loss of urate
transport activity.We determined the IC50 of iodine at 30uM concentration.
In radioactive up-take experiments iodinehad noeffect on uric acid transport.
Conclusions: In vitro the “materno-fetal” transport of uric acid is slow. This
indicates that in vivo the child is protected from short-term fluctuations of
maternal uric acid serum concentrations. The different results regarding
iodine-mediated regulation of GLUT9 transport activity between electrophysiological
and radioactive ligand uptake experiments may suggest that
iodine does not directly inhibit uric acid transport, but changes the mode
of up-take from an electrogenic to an electroneutral transport. GLUT9 is
not an uric acid uniporter, there are more ions involved in the transport.
This may allow regulating uric acid transport by the change from an active
to a passive transport.
Item Type: |
Conference or Workshop Item (Abstract) |
|---|---|
Division/Institute: |
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, Fine, Michael, Marini, Camilla, Clemençon, Benjamin, Albrecht, Christiane, Hediger, Matthias, Surbek, Daniel, Baumann, Marc |
Subjects: |
500 Science > 570 Life sciences; biology 600 Technology > 610 Medicine & health |
ISSN: |
0143-4004 |
Publisher: |
Elsevier |
Language: |
English |
Submitter: |
Barbara Franziska Järmann-Bangerter |
Date Deposited: |
02 Apr 2015 14:24 |
Last Modified: |
02 Mar 2023 23:26 |
BORIS DOI: |
10.7892/boris.67498 |
URI: |
https://boris.unibe.ch/id/eprint/67498 |
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