Detection of soluble E-selectin, ICAM-1, VCAM-1, and L-selectin in the cerebrospinal fluid of patients after subarachnoid hemorrhage

Polin, Richard S.; Bavbek, Murad; Shaffrey, Mark E.; Billups, Kevin L.; Bogaev, Christopher A.; Kassell, Neal F.; Lee, Kevin M.

doi:10.3171/jns.1998.89.4.0559

Cited by 169 publications

(98 citation statements)

References 51 publications

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“…There was no statistically significant correlation between E-selectin concentrations and the clinical profile of the patients, consistent with previous human SAH studies related to E-selectin (35,36). Nevertheless, we think that this may be due to the small number of patients studied here.…”

Section: Selectins In Subarachnoid Hemorrhagesupporting

confidence: 69%

“…The role of CAMs, principally selectins, in SAH is less clear and few studies have investigated the changes in selectin molecules in aneurysmal SAH (35,36). Polin et al (35) showed marked elevation of soluble forms of Eselectin in the CSF of 17 patients with ruptured SAH compared with levels in the CSF of 16 controls, patients with unruptured aneurysms, and patients tested months after the occurrence of SAH. In addition, 3 patients with angiographically demonstrated VS showed higher levels of E-selectin than the average for all other SAH patients.…”

Section: Selectins In Subarachnoid Hemorrhagementioning

confidence: 99%

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Serum and cerebrospinal fluid concentrations of E-selectin in patients with aneurysmal subarachnoid hemorrhage

Tanrıverdi

Sanuş

Ulu

et al. 2005

Braz J Med Biol Res

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The goal of the present study was to determine concentrations of Eselectin in both cerebrospinal fluid (CSF) and serum of patients with aneurysmal subarachnoid hemorrhage (SAH) and to evaluate the correlation between the clinical parameters and E-selectin levels. Both CSF and serum samples obtained from 12 patients with aneurysmal SAH and 8 patients with hydrocephalus (control group) without any other known central nervous system disease were assayed for Eselectin by quantitative enzyme-linked immunosorbent assay and the results were compared between the two groups. Mean levels of soluble forms of E-selectin within the first 3 days and on the 5th and 7th days of SAH were 4.0 ± 7.9, 2.8 ± 5.2, and 3.1 ± 4.9 ng/ml in the patient's CSF, and 33.7 ± 9.2, 35.1 ± 7.0, and 35.2 ± 8.7 ng/ml in serum, respectively. In contrast, mean E-selectin levels were 0.1 ± 0.2 ng/ml in CSF and 8.7 ± 5.0 ng/ml in serum of control patients. The difference between groups was statistically significant regarding both CSF and serum E-selectin levels (P < 0.05). Thus, we have demonstrated a marked increase of E-selectin concentration in both CSF and serum of patients with aneurysmal SAH compared with control and suggest that blocking the interaction between E-selectin and vascular endothelium may have a beneficial effect on vasospasms.

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Section: Selectins In Subarachnoid Hemorrhagesupporting

confidence: 69%

Section: Selectins In Subarachnoid Hemorrhagementioning

confidence: 99%

Serum and cerebrospinal fluid concentrations of E-selectin in patients with aneurysmal subarachnoid hemorrhage

Tanrıverdi

Sanuş

Ulu

et al. 2005

Braz J Med Biol Res

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“…This observation suggests that the recruitment of inflammatory cells into the subarachnoid environment may play an important role. Three adhesion molecules (E-selectin, ICAM-1, VCAM-1) were found to be elevated in CSF in patients having recently suffered an aneurismal SAH, with severely increased levels of E-selectin in those who later developed clinical VS (218). Expression of ICAM-1 was found to be increased in rat basilar artery not only in the endothelial layer but also in the media at 2 -5 days after SAH (219).…”

Section: Adhesion Molecule Expressionmentioning

confidence: 91%

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Sercombe

Dinh

Gomis

2002

Japanese Journal of Pharmacology

182

140

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ABSTRACT-Aneurysmal subarachnoid hemorrhage frequently results in complications including intracranial hypertension, rebleeding and vasospasm. The extravasated blood is responsible for a cascade of reactions involving release of various vasoactive and pro-inflammatory factors (several of which are purported to induce vasospasm) from blood and vascular components in the subarachnoid space. The authors review the available evidence linking these factors to the development of inflammatory lesions of the cerebral vasculature, emphasizing: 1) neurogenic inflammation due to massive release of sensory nerve neuropeptides; 2) hemoglobin from lysed erythrocytes, which creates functional lesions of endothelial and smooth muscle cells; 3) activity, expression and metabolites of lipoxygenases cyclooxygenases and nitric oxide synthases; 4) the possible role of endothelin-1 as a pro-inflammatory agent; 5) serotonin, histamine and bradykinin which are especially involved in blood-brain barrier disruption; 6) the prothrombotic and pro-inflammatory action of complement and thrombin towards endothelium; 7) the multiple actions of activated platelets, including platelet-derived growth factor production; 8) the presence of perivascular and intramural macrophages and granulocytes and their interaction with adhesion molecules; 9) the evolution, origins, and effects of pro-inflammatory cytokines, especially IL-1, TNF-a and IL-6. Human and animal studies on the use of anti-inflammatory agents in subarachnoid hemorrhage include superoxide and other radical scavengers, lipid peroxidation inhibitors, iron chelators, NSAIDs, glucocorticoids, and serine protease inhibitors. Many animal studies claim reduced vasospasm, but these effects are not always confirmed in human trials, where symptomatic vasospasm and outcome are the major endpoints. Despite recent work on penetrating vessel constriction, there is a paucity of studies on inflammatory markers in the microcirculation.

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“…This may result in the transmigration of T-cells and monocytes into the vessel wall (De Martin et al, 2000). In addition, both NF-kB and VCAM-1 have been shown to be involved in the pathogenesis of CVS after SAH (Kaynar et al, 2004;Polin et al, 1998;Zhou et al, 2007). The intracellular Ca 2 + concentration regulates the function of the endothelial barrier between blood and the surrounding tissue.…”

Section: Introductionmentioning

confidence: 99%

Cytosolic Ca²⁺Oscillations in Human Cerebrovascular Endothelial Cells after Subarachnoid Hemorrhage

Scharbrodt

Abdallah

Kasseckert

et al. 2008

J Cereb Blood Flow Metab

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Molecular mechanisms of cerebral vasospasm after subarachnoid hemorrhage (SAH) include specific modes of cell signaling like activation of nuclear factor (NF)-jB and vascular cell adhesion molecules (VCAM)-1 expression. The study's hypothesis is that cisternal cerebral spinal fluid (CSF) from patients after SAH may cause Ca 2 + oscillations which induce these modes of vascular inflammation in an in vitro model of human cerebral endothelial cells (HCECs). HCECs were incubated with cisternal CSF from 10 SAH patients with confirmed cerebral vasospasm. The CSF was collected on days 5 and 6 after hemorrhage. Cytosolic Ca 2 + concentrations and cell contraction as an indicator of endothelial barrier function were examined by fura-2 microflurometry. Activation of NF-jB and VCAM-1 expression were measured by immunocytochemistry. Incubation of HCEC with SAH-CSF provoked cytosolic Ca 2 + oscillations (0.31±0.09 per min), cell contraction, NF-jB activation, and VCAM-1 expression, whereas exposure to native CSF had no significant effect. When endoplasmic reticulum (ER) Ca 2 + -ATPase and ER inositol trisphosphate (IP3)-sensitive Ca 2 + channels were blocked by thapsigargin or xestospongin, the frequency of the Ca 2 + oscillations was reduced significantly. In analogy to the reduction of Ca 2 + oscillation frequency, the blockers impaired HCEC contraction, NF-jB activation, and VCAM-1 expression. Cisternal SAH-CSF induces cytosolic Ca 2 + oscillations in HCEC that results in cellular constriction, NF-jB activation, and VCAM-1 expression. The Ca 2 + oscillations depend on the function of ER Ca 2 + -ATPase and IP3-sensitive Ca 2 + channels.

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Detection of soluble E-selectin, ICAM-1, VCAM-1, and L-selectin in the cerebrospinal fluid of patients after subarachnoid hemorrhage

Cited by 169 publications

References 51 publications

Serum and cerebrospinal fluid concentrations of E-selectin in patients with aneurysmal subarachnoid hemorrhage

Serum and cerebrospinal fluid concentrations of E-selectin in patients with aneurysmal subarachnoid hemorrhage

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Cytosolic Ca²⁺Oscillations in Human Cerebrovascular Endothelial Cells after Subarachnoid Hemorrhage

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Detection of soluble E-selectin, ICAM-1, VCAM-1, and L-selectin in the cerebrospinal fluid of patients after subarachnoid hemorrhage

Cited by 169 publications

References 51 publications

Serum and cerebrospinal fluid concentrations of E-selectin in patients with aneurysmal subarachnoid hemorrhage

Serum and cerebrospinal fluid concentrations of E-selectin in patients with aneurysmal subarachnoid hemorrhage

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Cytosolic Ca2+Oscillations in Human Cerebrovascular Endothelial Cells after Subarachnoid Hemorrhage

Contact Info

Product

Resources

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Cytosolic Ca²⁺Oscillations in Human Cerebrovascular Endothelial Cells after Subarachnoid Hemorrhage