Repression of adenosine triphosphate–binding cassette transporter ABCG2 by estrogen increases intracellular glutathione in brain endothelial cells following ischemic reperfusion injury

Shin, Jeong-Ah; Jeong, Sae Im; Kim, Hye Won; Jang, Gyeonghui; Ryu, Dong Ryeol; Ahn, Young Ho; Choi, Ji Ha; Choi, Youn Hee; Park, Eun Mi

doi:10.1016/j.neurobiolaging.2018.02.020

Cited by 6 publications

(5 citation statements)

References 49 publications

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“…Bisphenol A decreased Abcg2 protein and activity levels in isolated rat brain capillaries via an ER α -dependent genomic pathway ( Nickel and Mahringer, 2014 ). Specifically, upon bisphenol A-mediated activation, ER α binds to the estrogen response element in the Abcg2 promotor where it acts as a negative regulator resulting in a slow decrease in Abcg2 expression and activity levels in isolated mouse brain capillaries ( Zhang et al, 2010 ; Shin et al, 2018 ). Phytoestrogens from soybeans also induce ABCG2 expression and protein activity through a genomic signaling pathway in breast cancer cell lines ( Rigalli et al, 2019a , b ).…”

Section: Regulation Of Abcb1/abcg2 At the Blood-brain Barriermentioning

confidence: 99%

ABCB1 and ABCG2 Regulation at the Blood-Brain Barrier: Potential New Targets to Improve Brain Drug Delivery

2023

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Section: Regulation Of Abcb1/abcg2 At the Blood-brain Barriermentioning

confidence: 99%

ABCB1 and ABCG2 Regulation at the Blood-Brain Barrier: Potential New Targets to Improve Brain Drug Delivery

2023

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“…For example, P‐glycoprotein (P‐gp/MDR1/ABCB1), a particularly important ABC transporter that is responsible for handling a wide variety of endogenous substrates and xenobiotics, is upregulated after ischemic stroke in rodents (Cen et al, ; Cui et al, ; Spudich et al, ). The breast cancer resistant protein (BCRP/ABCG2) expression is also increased in the peri‐infarct areas (Dazert et al, ; Shin et al, ).…”

Section: The Neonatal Neurovascular Unit In Hypoxic‐ischemic Conditionsmentioning

confidence: 99%

“…The breast cancer resistant protein (BCRP/ABCG2) expression is also increased in the peri-infarct areas (Dazert et al, 2006;Shin et al, 2018).…”

Section: Transport System Dysfunctionmentioning

confidence: 99%

Hypoxic‐ischemic‐related cerebrovascular changes and potential therapeutic strategies in the neonatal brain

Disdier

Stonestreet

2020

J of Neuroscience Research

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Perinatal hypoxic‐ischemic (HI)‐related brain injury is an important cause of morbidity and long‐standing disability in newborns. The only currently approved therapeutic strategy available to reduce brain injury in the newborn is hypothermia. Therapeutic hypothermia can only be used to treat HI encephalopathy in full‐term infants and survivors remain at high risk for a wide spectrum of neurodevelopmental abnormalities as a result of residual brain injury. Therefore, there is an urgent need for adjunctive therapeutic strategies. Inflammation and neurovascular damage are important factors that contribute to the pathophysiology of HI‐related brain injury and represent exciting potential targets for therapeutic intervention. In this review, we address the role of each component of the neurovascular unit (NVU) in the pathophysiology of HI‐related injury in the neonatal brain. Disruption of the blood–brain barrier (BBB) observed in the early hours after an HI‐related event is associated with a response at the basal lamina level, which comprises astrocytes, pericytes, and immune cells, all of which could affect BBB function to further exacerbate parenchymal injury. Future research is required to determine potential drugs that could prevent or attenuate neurovascular damage and/or augment repair. However, some studies have reported beneficial effects of hypothermia, erythropoietin, stem cell therapy, anti‐cytokine therapy and metformin in ameliorating several different facets of damage to the NVU after HI‐related brain injury in the perinatal period.

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“…via ATP-biding cassette (ABC) transporters) has an important role in regulating both the brain concentrations of endogenous compounds and xenobiotics, there is great interest in how such transport is regulated. Recent examples include reports by Hartz et al [45], who found that preventing P-glycoprotein ubiquitination could be used to decrease β-amyloid levels in a mouse model of Alzheimer’s disease; Xie et al [46] who provide evidence that microRNA-298 regulates P-glycoprotein; and Shin et al [47] who showed that estrogen represses breast cancer resistance protein expression and activity in brain endothelial cells after ischemia. One neglected aspect of blood–brain transport studies is whether there may be sex differences.…”

Section: Brain Endotheliummentioning

confidence: 99%

The year in review: progress in brain barriers and brain fluid research in 2018

Keep

Jones²,

Drewes

2019

Fluids Barriers CNS

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This editorial focuses on the progress made in brain barrier and brain fluid research in 2018. It highlights some recent advances in knowledge and techniques, as well as prevalent themes and controversies. Areas covered include: modeling, the brain endothelium, the neurovascular unit, the blood–CSF barrier and CSF, drug delivery, fluid movement within the brain, the impact of disease states, and heterogeneity.

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Repression of adenosine triphosphate–binding cassette transporter ABCG2 by estrogen increases intracellular glutathione in brain endothelial cells following ischemic reperfusion injury

Cited by 6 publications

References 49 publications

ABCB1 and ABCG2 Regulation at the Blood-Brain Barrier: Potential New Targets to Improve Brain Drug Delivery

ABCB1 and ABCG2 Regulation at the Blood-Brain Barrier: Potential New Targets to Improve Brain Drug Delivery

Hypoxic‐ischemic‐related cerebrovascular changes and potential therapeutic strategies in the neonatal brain

The year in review: progress in brain barriers and brain fluid research in 2018

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