gms | German Medical Science

59th Annual Meeting of the German Society of Neurosurgery (DGNC)
3rd Joint Meeting with the Italian Neurosurgical Society (SINch)

German Society of Neurosurgery (DGNC)

1 - 4 June 2008, Würzburg

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Subarachnoid hemorrhage induces cytosolic Ca2+-oscillations in human cerebrovascular endothelial cells

Induktion von zytosolischen Ca2+-Oszillationen in humanen zerebralen Endothelzellen nach subarachnoidaler Blutung

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  • corresponding author W. Scharbrodt - Neurochirurgische Klinik, Universitätsklinikum Gießen
  • Y. Abdallah - Physiologisches Institut, Universität Gießen
  • S. A. Kasseckert - Physiologisches Institut, Universität Gießen
  • D. Gligorievski - Physiologisches Institut, Universität Gießen
  • H. M. Piper - Physiologisches Institut, Universität Gießen
  • D.-K. Böker - Neurochirurgische Klinik, Universitätsklinikum Gießen
  • W. Deinsberger - Neurochirurgische Klinik, Universitätsklinikum Gießen
  • M. F. Oertel - Neurochirurgische Klinik, Universitätsklinikum Gießen

Deutsche Gesellschaft für Neurochirurgie. Società Italiana di Neurochirurgia. 59. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3. Joint Meeting mit der Italienischen Gesellschaft für Neurochirurgie (SINch). Würzburg, 01.-04.06.2008. Düsseldorf: German Medical Science GMS Publishing House; 2008. DocP 065

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2008/08dgnc334.shtml

Published: May 30, 2008

© 2008 Scharbrodt et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

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Objective: Molecular mechanisms of vascular inflammation include specific modes of cell signaling like endothelial cytosolic Ca2+-oscillations that activate NF-κB, lead to VCAM-1 expression and cell contraction. The goal of this study was to investigate this pathophysiological sequence of events in vitro on human cerebral endothelial cells (HCEC) which were exposed to cisternal cerebrospinal fluid (CSF) from patients, after aneurysmal subarachnoid hemorrhage (SAH).

Methods: HCEC were incubated with cisternal CSF from 10 SAH patients with cerebral vasospasm. CSF was collected on the 5th and 6th day after SAH. Cytosolic Ca2+-concentrations and cell contraction were examined by Fura-2 microfluometry. Thapsigargin, xestospongin and ryanidine were used to block endoplasmic reticulum (ER) ATPase, inositol-triphosphate (IP3) and ryanidine-dependent Ca2+-channels, respectively. NF-κB and VCAM-1 activation was measured immunocytochemically.

Results: Incubation of HCEC with SAH-CSF provoked cytosolic Ca2+ oscillations (0.31±0.09 min-1) and cell contraction. No Ca2+-oscillations were detected after exposure to native CSF. The presence of thapsigargin or xestospongin significantly reduces the frequency of Ca2+ oscillations and cell contraction whereas ryanodine had no influence. Incubation of HCEC with SAH-CSF induced NF-κB activation and VCAM-1 expression, which were significantly reduced by thapsigargin or xestospongin

Conclusions: Cisternal CSF from SAH patients induces intercellular gap-formation, NF-κB activation and VCAM-1 expression as key factors of vascular inflammation. This is due to cytosolic Ca2+oscillations in HCEC as a result of a dysfunction of the ER.