Characterization of microvascular basal lamina damage and blood–brain barrier dysfunction following subarachnoid hemorrhage in rats

Schöller, Karsten; Trinkl, A.; Kłopotowski, Mariusz; Thal, Serge C.; Plesnila, Nikolaus; Trabold, Raimund; Hamann, Gerhard F.; Schmid-Elsaesser, Robert; Zausinger, Stefan

doi:10.1016/j.brainres.2007.01.034

Cited by 92 publications

(78 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…4 Moreover, it was recently shown that acute METH treatment causes BBB disruption. 10 Herein, we used albumin staining as a marker for BBB disruption 30 since this is a blood serum protein that does not cross the BBB under normal conditions. Moreover, collagen IV is one of the most expressed proteins in basal lamina and is responsible for the mechanical support of ECs.…”

Section: Methamphetamine Impairs the Barrier Function Of Endothelial mentioning

confidence: 99%

“…Moreover, collagen IV is one of the most expressed proteins in basal lamina and is responsible for the mechanical support of ECs. 30 Thus, considering the crucial role of striatum in METH addiction and neurotoxicity, 4 we further investigated the alterations in collagen IV expression and the presence of albumin Figure 2. Methamphetamine (METH) impairs barrier properties via tumor necrosis factor-alpha (TNF-α)/nuclear factor-kappa B (NF-κB) pathway.…”

Section: Methamphetamine Impairs the Barrier Function Of Endothelial mentioning

confidence: 99%

See 1 more Smart Citation

The TNF-α/Nf-κB Signaling Pathway has a Key Role in Methamphetamine–Induced Blood–Brain Barrier Dysfunction

Coelho-Santos

Leitão

Cardoso

et al. 2015

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Methamphetamine (METH) is a psychostimulant that causes neurologic and psychiatric abnormalities. Recent studies have suggested that its neurotoxicity may also result from its ability to compromise the blood-brain barrier (BBB). Herein, we show that METH rapidly increased the vesicular transport across endothelial cells (ECs), followed by an increase of paracellular transport. Moreover, METH triggered the release of tumor necrosis factor-alpha (TNF-α), and the blockade of this cytokine or the inhibition of nuclear factor-kappa B (NF-κB) pathway prevented endothelial dysfunction. Since astrocytes have a crucial role in modulating BBB function, we further showed that conditioned medium obtained from astrocytes previously exposed to METH had a negative impact on barrier properties also via TNF-α/NF-κB pathway. Animal studies corroborated the in vitro results. Overall, we show that METH directly interferes with EC properties or indirectly via astrocytes through the release of TNF-α and subsequent activation of NF-κB pathway culminating in barrier dysfunction.

show abstract

Section: Methamphetamine Impairs the Barrier Function Of Endothelial mentioning

confidence: 99%

Section: Methamphetamine Impairs the Barrier Function Of Endothelial mentioning

confidence: 99%

The TNF-α/Nf-κB Signaling Pathway has a Key Role in Methamphetamine–Induced Blood–Brain Barrier Dysfunction

Coelho-Santos

Leitão

Cardoso

et al. 2015

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

show abstract

“…The source of LDL at the subendothelial layer might be circulating blood. The blood-arterial wall barrier in the major cerebral arteries is disrupted by SAH, which can allow penetration of plasma components into the vessel wall 30,38,40 (Fig. 6A).…”

Section: Discussionmentioning

confidence: 99%

“…5,11 Procyanidin is immediately absorbed after ingestion, and the blood concentration increases within 1 hour in a dose-dependent manner. 25 After being absorbed in blood, it is distributed to various tissues and organs, including the brain, within several hours of ingestion, 40 which suggests that procyanidins can pass the blood-brain barrier. The dosage of apple polyphenol administered in the lowdose group in this study was 10 mg/kg, which is the same as the dose per body weight used in the study investigating the usefulness of apple polyphenol in the primary prevention of metabolic syndrome.…”

Section: Discussionmentioning

confidence: 99%

Role of oxidized LDL and lectin-like oxidized LDL receptor-1 in cerebral vasospasm after subarachnoid hemorrhage

Matsuda¹,

Ohkuma²,

Naraoka³

et al. 2014

JNS

View full text Add to dashboard Cite

T he consequences of subarachnoid hemorrhage (SAH) after cerebral aneurysm rupture are devastating, with mortality rates as high as 50% and the majority of survivors left with moderate to severe disability. 15 Cerebral vasospasm causes cerebral ischemia and is a major contributor to the high morbidity and mortality rates associated with SAH. The pathogenesis of cerebral vasospasm, however, has not been fully clarified, and potential preventative therapies for this phenomenon have not been established. 7,8,17 Oxyhemoglobin derived from a subarachnoid clot and the free radicals subsequently generated have been considered important causes of cerebral vasospasm. 22,24,33,43 These radicals, by means of a scavenging effect, may be related to cerebral vasospasm by suppressing nitric ox- Object. Cerebral vasospasm after subarachnoid hemorrhage (SAH) is a serious complication. Free radicals derived from subarachnoid clotting are recognized to play an important role. Oxidized low-density lipoprotein (ox-LDL) and lectin-like oxidized LDL receptor-1 (LOX-1) have been shown to be related to the pathogenesis of atherosclerosis and may increase in cerebral arteries after SAH, due to the action of free radicals derived from a subarachnoid clot. These molecules may also affect the pathogenesis of vasospasm, generating intracellular reactive oxygen species and downregulating the expression of endothelial NO synthase (eNOS). If so, apple polyphenol might be effective in the prevention of vasospasm due to an abundant content of procyanidins, which exhibit strong radical scavenging effects, and the ability to suppress ox-LDL and LOX-1. The purposes of this study were to investigate changes in levels of ox-LDL and LOX-1 after SAH and whether administering apple polyphenol can modify cerebral vasospasm.Methods. Forty Japanese white rabbits were assigned randomly to 4 groups: an SAH group (n = 10); a shamoperation group (n = 10), which underwent intracisternal saline injection; a low-dose polyphenol group (n = 10) with SAH and oral administration of apple polyphenol at 10 mg/kg per day from Day 0 to Day 3; and a high-dose polyphenol group (n = 10) with SAH and oral administration of apple polyphenol at 50 mg/kg per day. At Day 4, the basilar artery and brain was excised from each rabbit. The degree of cerebral vasospasm was evaluated by measuring the cross-sectional area of each basilar artery, and the expression of ox-LDL, LOX-1, and eNOS was examined for each basilar artery by immunohistochemical staining and reverse transcriptase polymerase chain reaction. In addition, neuronal apoptosis in the cerebral cortex was evaluated by TUNEL.Results. Compared with the sham group, the expression of ox-LDL and LOX-1 in the basilar arterial wall was significantly increased in the SAH group, the expression of eNOS was significantly decreased, and the cross-sectional area of basilar artery was significantly decreased. Compared with the SAH group, the cross-sectional area of basilar artery was increased in the polyphenol groups, together with the ...

show abstract

“…3,8,9 After SAH, a global reduction in cerebral perfusion due to early vasoconstriction of the microvasculature and increased intracranial pressure due to the volume effect of extravascular blood are thought to result in cerebral ischemia and blood-brain barrier disruption with a consecutive increase in cerebral water content. 14,17,21 This finding is important because brain edema is associated with a poor outcome in SAH; therefore, preventing this complication could improve patient recovery.3 Severe cell swelling, characteristic of cytotoxic edema, can restrict the diffusion of substances in the interstitial fluid, leading to intracranial hypertension as the volume of the brain parenchyma increases to occupy a larger fraction of the cranial volume. The sulfonic amino acid taurine plays an important role in the regulation of cell volume in cultured neurons and glia.…”

mentioning

confidence: 99%

Plasma taurine as a predictor of poor outcome in patients with mild neurological deficits after aneurysmal subarachnoid hemorrhage

Coll¹,

Pérez-Neri

Avendaño³

et al. 2013

JNS

View full text Add to dashboard Cite

Object. The object of this study was to determine the relationship between plasma taurine and subarachnoid hemorrhage (SAH) outcome.Methods. Forty patients with SAH and mild neurological deficits were included in this prospective, blinded cohort study. Plasma taurine levels were measured using high-performance liquid chromatography on admission and were correlated with patient outcomes at discharge.Results. Twenty-five percent of the patients ultimately had a poor outcome. Plasma taurine concentrations at admission were increased (2-fold) in SAH patients with a favorable outcome and were further increased (6-fold) in those who had a poor outcome. Increased taurine levels identified patients who would be discharged with a poor outcome, with sensitivity and specificity values of approximately 80% and 100%, respectively, and positive and negative predictive values of approximately 90%. Delayed cerebral vasospasm showed an OR of 27.9 (95% CI 1.090-714.9) for a poor outcome, whereas an increased taurine concentration had an OR of 105 for a poor outcome (95% CI 8.3-1328.0, p < 0.001).Conclusions. Increased plasma taurine concentrations on admission predict a poor outcome in SAH. J. Barges-Coll et al. 1022J Neurosurg / Volume 119 / October 2013 come predictor for Grades IV and V, but patients with a mild neurological deficit may unexpectedly have a poor outcome. 22 Up to 55% of patients with Fisher Grades 2 or 3 may have a poor outcome. 10,20 It is possible that the plasma taurine concentration may be elevated from the onset of SAH and may be associated with patient outcome, reflecting possible brain edema and explaining the unexpectedly poor outcome of patients with a mild neurological deficit after SAH. 17 Methods Study ParticipantsIn this prospective, blinded cohort study, approved by our institutional review board, we considered 211 consecutive patients who were admitted to the Emergency Department of our institute under the suspected diagnosis of a ruptured aneurysm (Fig. 1). Among these patients, only 41 fulfilled our study inclusion criteria: admission within the first 24 hours after SAH onset, HH Grade I-II, WFNS Grade I-II, 8 hours of fasting, not referred from another hospital, taking no medication during the previous 8 hours, and willingness to participate in the study and sign informed consent. One patient was excluded from the final analysis since taurine analysis was inconclusive. Data pertaining to demographic factors, comorbidities, Glasgow Coma Scale score, and HH grade were recorded on admission to the Emergency Department. Eighteen healthy volunteers were recruited as the control group.Routine blood analyses were performed (complete blood count, glucose, electrolytes, partial thromboplastin time, international normalized ratio). All patients underwent a 4-vessel digital angiography and CT study for the diagnosis of a ruptured aneurysm. Sample ProcessingA 20-ml blood sample was taken from every patient upon admission to the Emergency Department. Samples were labeled with a serial number and taken t...

show abstract

Characterization of microvascular basal lamina damage and blood–brain barrier dysfunction following subarachnoid hemorrhage in rats

Cited by 92 publications

References 47 publications

The TNF-α/Nf-κB Signaling Pathway has a Key Role in Methamphetamine–Induced Blood–Brain Barrier Dysfunction

The TNF-α/Nf-κB Signaling Pathway has a Key Role in Methamphetamine–Induced Blood–Brain Barrier Dysfunction

Role of oxidized LDL and lectin-like oxidized LDL receptor-1 in cerebral vasospasm after subarachnoid hemorrhage

Plasma taurine as a predictor of poor outcome in patients with mild neurological deficits after aneurysmal subarachnoid hemorrhage

Contact Info

Product

Resources

About