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Tytuł pozycji:

Kidney Ischemia/Reperfusion Injury Induces Changes in the Drug Transporter Expression at the Blood–Brain Barrier in vivo and in vitro

Tytuł :
Kidney Ischemia/Reperfusion Injury Induces Changes in the Drug Transporter Expression at the Blood–Brain Barrier in vivo and in vitro
Autorzy :
Malgorzata Burek
Sandra Burmester
Ellaine Salvador
Kerstin Möller-Ehrlich
Reinhard Schneider
Norbert Roewer
Michiaki Nagai
Carola Y. Förster
Pokaż więcej
Temat :
kidney ischemia/reperfusion injury
brain pathology
blood–brain barrier
drug transporter
tight junctions
Physiology
QP1-981
Źródło :
Frontiers in Physiology, Vol 11 (2020)
Wydawca :
Frontiers Media S.A., 2020.
Rok publikacji :
2020
Kolekcja :
LCC:Physiology
Typ dokumentu :
article
Opis pliku :
electronic resource
Język :
English
ISSN :
1664-042X
Relacje :
https://www.frontiersin.org/articles/10.3389/fphys.2020.569881/full; https://doaj.org/toc/1664-042X
DOI :
10.3389/fphys.2020.569881
Dostęp URL :
https://doaj.org/article/982451a64bec4ea3af376b23b21e1fe7
Numer akcesji :
edsdoj.982451a64bec4ea3af376b23b21e1fe7
Czasopismo naukowe
Ischemia/reperfusion injury is a major cause of acute kidney injury (AKI). AKI is characterized by a sudden decrease in kidney function, systemic inflammation, oxidative stress, and dysregulation of the sodium, potassium, and water channels. While AKI leads to uremic encephalopathy, epidemiological studies have shown that AKI is associated with a subsequent risk for developing stroke and dementia. To get more insights into kidney–brain crosstalk, we have created an in vitro co-culture model based on human kidney cells of the proximal tubule (HK-2) and brain microvascular endothelial cells (BMEC). The HK-2 cell line was grown to confluence on 6-well plates and exposed to oxygen/glucose deprivation (OGD) for 4 h. Control HK-2 cells were grown under normal conditions. The BMEC cell line cerebED was grown to confluence on transwells with 0.4 μm pores. The transwell filters seeded and grown to confluence with cereEND were inserted into the plates with HK-2 cells with or without OGD treatment. In addition, cerebEND were left untreated or treated with uremic toxins, indole-3-acetic acid (IAA) and indoxyl sulfate (IS). The protein and mRNA expression of selected BBB-typical influx transporters, efflux transporters, cellular receptors, and tight junction proteins was measured in BMECs. To validate this in vitro model of kidney–brain interaction, we isolated brain capillaries from mice exposed to bilateral renal ischemia (30 min)/reperfusion injury (24 h) and measured mRNA and protein expression as described above. Both in vitro and in vivo systems showed similar changes in the expression of drug transporters, cellular receptors, and tight junction proteins. Efflux pumps, in particular Abcb1b, Abcc1, and Abcg2, have shown increased expression in our model. Thus, our in vitro co-culture system can be used to study the cellular mechanism of kidney and brain crosstalk in renal ischemia/reperfusion injury.

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