HIV‐1 gp120 as Well as Alcohol Affect Blood–Brain Barrier Permeability and Stress Fiber Formation: Involvement of Reactive Oxygen Species

Shiu, Carlum; Barbier, Élisabeth; Cello, Francescopaolo Di; Choi, Hee Jung; Stins, Monique F.

doi:10.1111/j.1530-0277.2006.00271.x

Cited by 60 publications

(55 citation statements)

References 43 publications

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“…In CNS, CCR5 expression has been identified in microglia and brain endothelial cells (28,(55)(56)(57)(58)(59). We and others had shown that CCR5 was normally expressed on brain endothelial cells at lower level (28,57).…”

Section: Discussionmentioning

confidence: 99%

Amyloid β Interaction with Receptor for Advanced Glycation End Products Up-Regulates Brain Endothelial CCR5 Expression and Promotes T Cells Crossing the Blood-Brain Barrier

Shang²,

Zhao³

et al. 2009

The Journal of Immunology

105

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How circulating T cells infiltrate into the brain in Alzheimer disease (AD) remains unclear. We previously reported that amyloid β (Aβ)-dependent CCR5 expression in brain endothelial cells is involved in T cell transendothelial migration. In this study, we explored the signaling pathway of CCR5 up-regulation by Aβ. We showed that inhibitors of JNK, ERK, and PI3K significantly decreased Aβ-induced CCR5 expression in human brain microvascular endothelial cells (HBMECs). Chromatin immunoprecipitation assay revealed that Aβ-activated JNK, ERK, and PI3K promoted brain endothelial CCR5 expression via transcription factor Egr-1. Furthermore, neutralization Ab of receptor for advanced glycation end products (RAGE; an Aβ receptor) effectively blocked Aβ-induced JNK, ERK, and PI3K activation, contributing to CCR5 expression in HBMECs. Aβ fails to induce CCR5 expression when truncated RAGE was overexpressed in HBMECs. Transendothelial migration assay showed that the migration of MIP-1α (a CCR5 ligand)-expressing AD patients’ T cells through in vitro blood-brain barrier model was effectively blocked by anti-RAGE Ab, overexpression of truncated RAGE, and dominant-negative PI3K, JNK/ERK, or Egr-1 RNA interference in HBMECs, respectively. Importantly, blockage of intracerebral RAGE abolished the up-regulation of CCR5 on brain endothelial cells and the increased T cell infiltration in the brain induced by Aβ injection in rat hippocampus. Our results suggest that intracerebral Aβ interaction with RAGE at BBB up-regulates endothelial CCR5 expression and causes circulating T cell infiltration in the brain in AD. This study may provide a new insight into the understanding of inflammation in the progress of AD.

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Section: Discussionmentioning

confidence: 99%

Amyloid β Interaction with Receptor for Advanced Glycation End Products Up-Regulates Brain Endothelial CCR5 Expression and Promotes T Cells Crossing the Blood-Brain Barrier

Shang²,

Zhao³

et al. 2009

The Journal of Immunology

105

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“…It decreases the expression of various TJPs, including occludin, ZO-1,and ZO-2,and increases the migration of monocytes into the CNS[134,135]. Gp 120 induces the production of reactive oxygen species (ROS) through NADPH to upregulate the expression of MMP2 and MMP9 in endothelial cells [136, 137]. Gp120 also interacts with neurons to decrease mitochondrial movement, resulting in mitochondrial dysfunction [125, 138].…”

Section: Role Of Hiv-1 Proteins In Neurotoxicitymentioning

confidence: 99%

An Overview of Human Immunodeficiency Virus Type 1-Associated Common Neurological Complications: Does Aging Pose a Challenge?

Nookala

Mitra

Chaudhari

et al. 2017

JAD

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With increasing survival of patients infected with human immunodeficiency virus type 1 (HIV-1), the manifestation of heterogeneous neurological complications is also increasing alarmingly in these patients. Currently, more than 30% of about 40 million HIV-1 infected people worldwide develop central nervous system (CNS)-associated dysfunction, including dementia, sensory, and motor neuropathy. Furthermore, the highly effective antiretroviral therapy has been shown to increase the prevalence of mild cognitive functions while reducing other HIV-1-associated neurological complications. On the contrary, the presence of neurological disorder frequently affects the outcome of conventional HIV-1 therapy. Although, both the children and adults suffer from the post-HIV treatment-associated cognitive impairment, adults, especially depending on the age of disease onset, are more prone to CNS dysfunction. Thus, addressing neurological complications in an HIV-1-infected patient is a delicate balance of several factors and requires characterization of the molecular signature of associated CNS disorders involving intricate cross-talk with HIV-1-derived neurotoxins and other cellular factors. In this review, we summarize some of the current data supporting both the direct and indirect mechanisms, including neuro-inflammation and genome instability in association with aging, leading to CNS dysfunction after HIV-1 infection, and discuss the potential strategies addressing the treatment or prevention of HIV-1-mediated neurotoxicity.

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“…Neurons and astroglial cells are sensitive to alcohol consumption, which promotes an apoptotic pathway of neurodegeneration. Endothelial cell apoptosis allows considering a possibility of the blood-brain barrier disfunction [18]. Despite the fact that the alcohol-induced oligodendroglial cell death has been reported previously [1], we were unable to confirm oligodendroglial damage underlying alcohol consumption.…”

Section: Discussionmentioning

confidence: 59%

Chronic alcohol abuse is implicated in the oxidative stress and the changes in the neurotrophic factor receptor expression in the human CNS

Skuja

Groma

Kleina

2012

PoA

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Alcohol abuse and alcoholism induce brain damage, and, in some cases, neurodegeneration. The pathogenesis of the alcohol-induced injury of the CNS is a complex process in which oxidative stress plays an essential role. Alcohol increases the formation of reactive oxygen species and affects the antioxidant defense system of the brain. It is well known that oxidative stress induces apoptosis in neurons, as well as in other cell types. Neurotropins and their receptors have a crucial role in neural regulation. The aim of this study is an overall analysis of the CNS neuronal and glial cell death and the oxidative status by the use of immunohistochemical methods.Three different CNS regions -cortical, subventricular and basal ganglia were analyzed in the autopsy samples obtained from 10 chronic alcohol abused patients. The immunohistochemical detection of oxidative damage was performed using anti-Cu/Zn SOD monoclonal antibody, neural activity -anti-NGFR (p75 NTR ) antibody, apoptosis -the TUNEL reaction. Both, quantitative and semiquantitative estimations were used for the evaluation of results. The subventricular zone was characterized by a negative (75%) and a moderate (25%) astroglial SOD1 expression, the basal ganglia region -by strong (43%), moderate (43%), and low (14%) neuronal and moderate (71%) and low (29%) astroglial SOD1 expression, whereas, the cortex -by strong (33%) and moderate (66%) neuronal and moderate (67%), low (17%) and negative (17%) astroglial expression. The SOD1 expression was not detected in oligodendroglia and ependymocytes. Brain regions showed variability in the apoptotic cell death rates. Neuronal TUNEL-positive staining in Chronic alcohol abuse is implicated … 369 basal ganglia was higher than in the cerebral cortex. TUNEL-positive astrocytes were detected in the white matter, more frequently in the basal ganglia region when compared to the cortex. The apoptosis marker was nearly absent in ependymal and oligodendroglial cells. The rate of TUNEL-positive cortex endothelial cells was detected at 7.9% level in the case of chronic alcohol abuse. Neuronal processes showed heterogeneous NGFR expression: in the cortex, basal ganglia and the subventricular zone (negative/low), whereas the subcortex and the white matter -moderate and moderate/strong, accordingly. Alcohol-induced CNS vulnerability is related to the increase in oxidative stress; furthermore, it suggests an increased risk of neurodegeneration for neuronal and glial cells.

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HIV‐1 gp120 as Well as Alcohol Affect Blood–Brain Barrier Permeability and Stress Fiber Formation: Involvement of Reactive Oxygen Species

Cited by 60 publications

References 43 publications

Amyloid β Interaction with Receptor for Advanced Glycation End Products Up-Regulates Brain Endothelial CCR5 Expression and Promotes T Cells Crossing the Blood-Brain Barrier

Amyloid β Interaction with Receptor for Advanced Glycation End Products Up-Regulates Brain Endothelial CCR5 Expression and Promotes T Cells Crossing the Blood-Brain Barrier

An Overview of Human Immunodeficiency Virus Type 1-Associated Common Neurological Complications: Does Aging Pose a Challenge?

Chronic alcohol abuse is implicated in the oxidative stress and the changes in the neurotrophic factor receptor expression in the human CNS

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