Breakdown of Blood-Brain and Blood-Spinal Cord Barriers During Acute Methamphetamine Intoxication: Role of Brain Temperature

Kiyatkin, Eugene A.; Sharma, Hari Shanker

doi:10.2174/1871527315666160920112445

Cited by 21 publications

(7 citation statements)

References 41 publications

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“…There are numerous cellular and molecular mechanisms related to the BSCB permeability increasing induced by SCI. Reactive oxygen species (ROS) presents an ordinary initiate for numerous downstream paths that plays a critical role in BSCB dysfunction such as matrix metalloproteinases (MMP) activation, TJ modification and oxidative damage 37 - 39 . MMP-9 is involved in secondary damage induced by SCI and the disruption of BSCB by degrading the Occludin and Claudin-5 protein, rendering the leaky of BSCB and admitting neurotoxic components and immune cell to access the microenvironment of injured spinal cord.…”

Section: Discussionmentioning

confidence: 99%

Dl-3-n-butylphthalide prevents the disruption of blood-spinal cord barrier via inhibiting endoplasmic reticulum stress following spinal cord injury

Zheng-Lin¹,

Zhou²,

Zhang³

et al. 2017

Int. J. Biol. Sci.

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After spinal cord injury (SCI), the destruction of blood-spinal cord barrier (BSCB) is shown to accelerate gathering of noxious blood-derived components in the nervous system, leading to secondary neurodegenerative damages. SCI activates endoplasmic reticulum stress (ER stress), which is considered to evoke secondary damages of neurons and glia. Recent evidence indicates that Dl-3-n-butylphthalide (NBP) has the neuroprotective effect in ischaemic brain injury, but whether it has protective effects on SCI or not is largely unclear. Here, we show that NBP prevented BSCB disruption after SCI via inhibition of ER stress. Following a moderate contusion injury of the T9 level of spinal cord, NBP was administered by oral gavage and further treated once a day. NBP significantly attenuated BSCB permeability and breakdown of adherens junction (AJ) and tight junction (TJ) proteins, then improved locomotion recovery following SCI. The protective role of NBP on BSCB disruption is associated with the restrain of ER stress caused by SCI. Furthermore, NBP considerably constrained the expression of ER stress-associated proteins and degradation of TJ and AJ in human brain microvascular endothelial cells (HBMECs) treated with TG. In conclusion, our results indicate that ER stress is associated with the disruption of BSCB integrity after injury, NBP attenuates BSCB disruption via inhibiting ER stress and improve functional recovery following SCI.

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Section: Discussionmentioning

confidence: 99%

Dl-3-n-butylphthalide prevents the disruption of blood-spinal cord barrier via inhibiting endoplasmic reticulum stress following spinal cord injury

Zheng-Lin¹,

Zhou²,

Zhang³

et al. 2017

Int. J. Biol. Sci.

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“…To be included, patients had to meet trauma activation criteria, have evidence of TBI on radiographic imaging (CT head), and be admitted to the surgical trauma intensive care unit (ICU). We excluded patients with conditions known to adversely influence the BBB: intoxication or substance disorder, [18][19][20] active infection or antibiotic use, 21,22 partial-or full-thickness burns to >15% of body surface area, 23 penetrating head injury, central nervous system malignancy, 24 and spinal cord injury. Information on demographic characteristics, mortality, ICU length of stay, ICU-free days, intracranial pathology, and injury severity score (ISS) was ascertained by chart review.…”

Section: Methodsmentioning

confidence: 99%

Exploring blood-brain barrier hyperpermeability and potential biomarkers in traumatic brain injury

Robinson

Tharakan

Lomas³

et al. 2020

Baylor University Medical Center Proceedings

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Blood-brain barrier breakdown and associated vascular hyperpermeability leads to vasogenic edema in traumatic brain injury (TBI). Tight junctions maintain blood-brain barrier integrity; their disruption in TBI holds significant promise for diagnosis and treatment. A controlled cortical impactor was used for TBI in mouse studies. Blood was collected 1 h after injury and sent for antibody microarray analysis. Twenty human subjects with radiographic evidence of TBI were enrolled and blood collected within 48 h of admission. Control subjects were individuals with nontrauma diagnoses. The subjects were matched by age and gender. Enzyme-linked immunosorbent assays were performed on each TBI and control sample for tight junction-associated proteins (TJPs), inflammatory markers, and S100b. Plasma was used to conduct in vitro monolayer permeability studies with human brain endothelial cells. S100b and the TJP occludin were significantly elevated in TBI plasma in both the murine and human studies. Monolayer permeability studies showed increased hyperpermeability in TBI groups. Plasma from TBI subjects increases microvascular hyperpermeability in vitro. TJPs in the blood may be a potential biomarker for TBI.

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“…METH abuse has become a worldwide issue in which 40% of global neuropsychological impairment has been found to be associated with its use [ 15 ]. Acute METH has also been shown to induce hyperthermia [ 16 , 17 ] and breakdown of the BBB [ 18 ]. Long term exposure to METH has been shown to be associated with neurodegeneration and cognitive impairment [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Meta-Analysis of Methamphetamine Modulation on Amyloid Precursor Protein through HMGB1 in Alzheimer’s Disease

Alabed

Zhou

Sariyer

et al. 2021

IJMS

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The deposition of amyloid-beta (Aβ) through the cleavage of amyloid-beta precursor protein (APP) is a biomarker of Alzheimer’s disease (AD). This study used QIAGEN Ingenuity Pathway Analysis (IPA) to conduct meta-analysis on the molecular mechanisms by which methamphetamine (METH) impacts AD through modulating the expression of APP. All the molecules affected by METH and APP were collected from the QIAGEN Knowledge Base (QKB); 78 overlapping molecules were identified. Upon simulation of METH exposure using the “Molecule Activity Predictor” feature, eight molecules were found to be affected by METH and exhibited activation relationships on APP expression at a confidence of p = 0.000453 (Z-score = 3.51, two-tailed). Core Analysis of these eight molecules identified High Mobility Group Box protein 1 (HMGB1) signaling pathway among the top 5 canonical pathways with most overlap with the 8-molecule dataset. Simulated METH exposure increased APP expression through HMGB1 at a confidence of p < 0.00001 (Z-score = 7.64, two-tailed). HMGB1 is a pathogenic hallmark in AD progression. It not only increases the production of inflammatory mediators, but also mediates the disruption of the blood-brain barrier. Our analyses suggest the involvement of HMGB1 signaling pathway in METH-induced modulation of APP as a potential casual factor of AD.

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Breakdown of Blood-Brain and Blood-Spinal Cord Barriers During Acute Methamphetamine Intoxication: Role of Brain Temperature

Cited by 21 publications

References 41 publications

Dl-3-n-butylphthalide prevents the disruption of blood-spinal cord barrier via inhibiting endoplasmic reticulum stress following spinal cord injury

Dl-3-n-butylphthalide prevents the disruption of blood-spinal cord barrier via inhibiting endoplasmic reticulum stress following spinal cord injury

Exploring blood-brain barrier hyperpermeability and potential biomarkers in traumatic brain injury

Meta-Analysis of Methamphetamine Modulation on Amyloid Precursor Protein through HMGB1 in Alzheimer’s Disease

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