Patak, Pauline; Jin, Fengyan; Schäfer, Simon; Metzen, Eric; Hermann, Dirk:
The ATP-binding cassette transporters ABCB1 and ABCC1 are not regulated by hypoxia in immortalised human brain microvascular endothelial cells
In: Experimental and Translational Stroke Medicine, Vol. 3 (2011), No. 12
2011article/chapter in journalOA Gold
MedicineFaculty of Medicine » Essen University Hospital » Clinic for NeurologyScientific institutes » Center of Medical Biotechnology (ZMB) Faculty of Medicine » Essen University Hospital » Institute of Physiology
Related: 1 publication(s)
Title in English:
The ATP-binding cassette transporters ABCB1 and ABCC1 are not regulated by hypoxia in immortalised human brain microvascular endothelial cells
Author:
Patak, Pauline;Jin, Fengyan;Schäfer, SimonUDE
LSF ID
12996
ORCID
0000-0001-7289-6000ORCID iD
Other
connected with university
;
Metzen, EricUDE
LSF ID
50408
ORCID
0000-0002-2740-3219ORCID iD
Other
connected with university
;
Hermann, DirkUDE
GND
124495648
LSF ID
50474
ORCID
0000-0003-0198-3152ORCID iD
Other
connected with university
Year of publication:
2011
Open Access?:
OA Gold
DuEPublico 1 ID
EVALuna Biblio ID
19582
PubMed ID
Note:
OA Förderung 2012
Language of text:
English

Abstract in English:

Background: ATP-binding cassette transporters at the blood-brain barrier are actively regulated upon ischemic stroke in a way that impedes the access of pharmacological compounds to the brain tissue. The luminal endothelial transporter ABCB1 was recently shown to be increased, whereas the abluminal transporter ABCC1 was decreased on ischemic brain capillaries. In vitro studies using epithelial cells suggested that ABCB1 is regulated during hypoxia in a hypoxia-inducible factor (HIF)-1a-dependent way. Methods: In order to investigate whether hypoxia might be responsible for the expression changes of ABCB1 and ABCC1 in the ischemic brain, the immortalised human brain microvascular endothelial cell line hCMEC/D3 was exposed to hypoxia (1%) or anoxia (0%). Cell lysates were analysed by Western blot to detect the protein expression of ABCB1, ABCC1, HIF-1a and HIF-2a. Results: During hypoxia, an accumulation of HIF-1a and HIF-2a was noticed in hCMEC/D3 cells that followed different time kinetics. Both HIF-1a and HIF-2a abundance increased within 4 h of hypoxia. HIF-1a levels decreased to below detection levels within 16 h of hypoxia, whereas HIF-2a remained elevated even after 48 h. No changes of ABCB1 and ABCC1 expression were detected, neither on the mRNA nor protein level. Conclusion: Our data suggests that other factors than