The Expression and Function of ABC Transporters at the Blood-Brain Barrier

2015 ◽  
pp. 172-214
Author(s):  
Wandong Zhang ◽  
Michelle Bamji-Mirza ◽  
Nina Chang ◽  
Arsalan Haqqani ◽  
Danica Stanimirovic
Keyword(s):  
Blood Brain Barrier ◽  
Abc Transporters ◽  
Brain Barrier ◽  
Blood Brain ◽  
And Function

scholarly journals Alterations in Expression and Function of ABC Family Transporters at Blood-Brain Barrier under Liver Failure and Their Clinical Significances

Pharmaceutics ◽  
2018 ◽  
Vol 10 (3) ◽  
pp. 102 ◽  
Author(s):  
Yilin Fan ◽  
Xiaodong Liu
Keyword(s):  
Endothelial Cells ◽  
Hepatic Encephalopathy ◽  
Liver Failure ◽  
Blood Brain Barrier ◽  
Abc Transporters ◽  
Brain Barrier ◽  
Blood Brain ◽  
Microvessel Endothelial Cells ◽  
Brain Microvessel ◽  
And Function

Liver failure is often associated with hepatic encephalopathy, due to dyshomeostasis of the central nervous system (CNS). Under physiological conditions, the CNS homeostasis is precisely regulated by the blood-brain barrier (BBB). The BBB consists of brain microvessel endothelial cells connected with a junctional complex by the adherens junctions and tight junctions. Its main function is to maintain brain homoeostasis via limiting the entry of drugs/toxins to brain. The brain microvessel endothelial cells are characterized by minimal pinocytotic activity, absent fenestrations, and highly expressions of ATP-binding cassette (ABC) family transporters (such as P-glycoprotein, breast cancer resistance protein and multidrug resistance-associated proteins). These ABC transporters prevent brain from toxin accumulation by pumping toxins out of brain. Accumulating evidences demonstrates that liver failure diseases altered the expression and function of ABC transporters at The BBB, indicating that the alterations subsequently affect drugs’ brain distribution and CNS activity/neurotoxicity. ABC transporters also mediate the transport of endogenous substrates across the BBB, inferring that ABC transporters are also implicated in some physiological processes and the development of hepatic encephalopathy. This paper focuses on the alteration in the BBB permeability, the expression and function of ABC transporters at the BBB under liver failure status and their clinical significances.

PET Tracers for Imaging of ABC Transporters at the Blood-Brain Barrier: Principles and Strategies

2016 ◽  
Vol 22 (38) ◽  
pp. 5779-5785 ◽  
Author(s):  
Gert Luurtsema ◽  
Philip Elsinga ◽  
Rudi Dierckx ◽  
Ronald Boellaard ◽  
Aren Waarde
Keyword(s):  
Blood Brain Barrier ◽  
Abc Transporters ◽  
Brain Barrier ◽  
Pet Tracers ◽  
Blood Brain

Structure and function of the blood–brain barrier

2010 ◽  
Vol 37 (1) ◽  
pp. 13-25 ◽  
Author(s):  
N. Joan Abbott ◽  
Adjanie A.K. Patabendige ◽  
Diana E.M. Dolman ◽  
Siti R. Yusof ◽  
David J. Begley
Keyword(s):  
Blood Brain Barrier ◽  
Structure And Function ◽  
Brain Barrier ◽  
Blood Brain ◽  
And Function

scholarly journals Pseudogene ACTBP2 increases blood–brain barrier permeability by promoting KHDRBS2 transcription through recruitment of KMT2D/WDR5 in Aβ1–42 microenvironment

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Qianshuo Liu ◽  
Xiaobai Liu ◽  
Defeng Zhao ◽  
Xuelei Ruan ◽  
Rui Su ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Molecular Mechanisms ◽  
Rna Binding ◽  
Vital Role ◽  
Brain Barrier ◽  
Blood Brain ◽  
Bbb Permeability ◽  
Novel Target ◽  
And Function

AbstractThe blood–brain barrier (BBB) has a vital role in maintaining the homeostasis of the central nervous system (CNS). Changes in the structure and function of BBB can accelerate Alzheimer’s disease (AD) development. β-Amyloid (Aβ) deposition is the major pathological event of AD. We elucidated the function and possible molecular mechanisms of the effect of pseudogene ACTBP2 on the permeability of BBB in Aβ1–42 microenvironment. BBB model treated with Aβ1–42 for 48 h were used to simulate Aβ-mediated BBB dysfunction in AD. We proved that pseudogene ACTBP2, RNA-binding protein KHDRBS2, and transcription factor HEY2 are highly expressed in ECs that were obtained in a BBB model in vitro in Aβ1–42 microenvironment. In Aβ1–42-incubated ECs, ACTBP2 recruits methyltransferases KMT2D and WDR5, binds to KHDRBS2 promoter, and promotes KHDRBS2 transcription. The interaction of KHDRBS2 with the 3′UTR of HEY2 mRNA increases the stability of HEY2 and promotes its expression. HEY2 increases BBB permeability in Aβ1–42 microenvironment by transcriptionally inhibiting the expression of ZO-1, occludin, and claudin-5. We confirmed that knocking down of Khdrbs2 or Hey2 increased the expression levels of ZO-1, occludin, and claudin-5 in APP/PS1 mice brain microvessels. ACTBP2/KHDRBS2/HEY2 axis has a crucial role in the regulation of BBB permeability in Aβ1–42 microenvironment, which may provide a novel target for the therapy of AD.

Overview of the Structure and Function of the Blood-Brain Barrier in vivo

2001 ◽  
pp. 1-7 ◽  
Author(s):  
Joseph D. Fenstermacher ◽  
Tavarekere Nagaraja ◽  
Kenneth R. Davies
Keyword(s):  
Blood Brain Barrier ◽  
Structure And Function ◽  
Brain Barrier ◽  
Blood Brain ◽  
And Function

scholarly journals The Drosophila blood-brain barrier: development and function of a glial endothelium

2014 ◽  
Vol 8 ◽  
Author(s):  
Stefanie Limmer ◽  
Astrid Weiler ◽  
Anne Volkenhoff ◽  
Felix Babatz ◽  
Christian Klämbt
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain ◽  
And Function
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