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70. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Skandinavischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

12.05. - 15.05.2019, Würzburg

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Cyclo-oxygenase 2 is expressed in the wall brain AVM vessels and associates with inflammation – a putative mediator of vessel wall remodeling in brain AVMs

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  • presenting/speaker Sara Keränen - Kuopio University Hospital, Hemorrhagic Brain Pathology Research Group, NeuroCenter, Kuopio, Finland; University of Eastern Finland, Dept of Molecular Medicine, AIV-Institute, Kuopio, Finland
  • Santeri Suutarinen - Kuopio University Hospital, Hemorrhagic Brain Pathology Research Group, NeuroCenter, Kuopio, Finland; University of Eastern Finland, Department of Molecular Medicine, AIV-Institute, Kuopio, Finland
  • Johanna Laakkkonen - University of Eastern Finland, Dept of Molecular Medicine, AIV-Institute, Kuopio, Finland
  • Diana Guo - UCSF, Center for Cerebrovascular Research, Dept of Anesthesiology and Perioperative Care, San Francisco, United States
  • Ludmila Pawlikowska - UCSF, Center for Cerebrovascular Research, Dept of Anesthesiology and Perioperative Care, San Francisco, United States
  • Behnam Rezai Jahromi - Kuopio University Hospital, Hemorrhagic Brain Pathology Research Group, NeuroCenter, Kuopio, Finland; University of Eastern Finland, Dept of Molecular Medicine, AIV-Institute, Kuopio, Finland
  • Tuomas Rauramaa - Kuopio University Hospital, Hemorrhagic Brain Pathology Research Group, NeuroCenter, Kuopio, Finland; Kuopio Universitätsklinikum and University of Eastern Finland, Dept of Pathology, Kuopio, Finland
  • Timo Krings - Universitätsklinikum Network Toronto, Dept of Neuroradiology, Toronto, Canada
  • Timo Koivisto - Kuopio University Hospital, Dept of Neurosurgery, NeuroCenter, Kuopio, Finland
  • Michael T. Lawton - Barrow Brain and Spine Institute, Dept of Neurosurgery, Phoenix, United States
  • Ivan Radovanovic - Universitätsklinikum Network Toronto, Dept of Neurosurgery, Toronto, Canada
  • Helen Kim - UCSF, Center for Cerebrovascular Research, Dept of Anesthesiology and Perioperative Care, San Francisco, United States
  • Marie Faughnan - Universitätsklinikum Network Toronto, Dept of Pulmonary Medicine, Toronto, Canada
  • Juhana Frösen - Kuopio University Hospital, Hemorrhagic Brain Pathology Research Group, NeuroCenter, Kuopio, Finland; University of Eastern Finland, Dept of Molecular Medicine, AIV-Institute, Kuopio, Finland; Kuopio University Hospital, Dept of Neurosurgery, NeuroCenter, Kuopio, Finland

Deutsche Gesellschaft für Neurochirurgie. 70. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Skandinavischen Gesellschaft für Neurochirurgie. Würzburg, 12.-15.05.2019. Düsseldorf: German Medical Science GMS Publishing House; 2019. DocJM-SNS07

doi: 10.3205/19dgnc245, urn:nbn:de:0183-19dgnc2451

Published: May 8, 2019

© 2019 Keränen et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

Text

Objective: Arteriovenous malformations in the brain (bAVM) may rupture causing severe disability or death. Currently there is no medical therapy to prevent AVM hemorrhage. BAVMs are characterized by abnormally high flow that has been shown to trigger degenerative expansive remodelling in other vessels. This inflammatory remodelling is mediated by cyclo-oxygenase -2 (COX2), an induced enzyme that is the target of non-steroidal anti-inflammatory drugs. Inflammation has been reported in bAVMs with pathological vessels growth and remodeling. We investigated whether COX2 is expressed in bAVMs and whether it associates with inflammation and haemorrhage in these lesions.

Methods: Tissue was obtained from surgery of 110 bAVMs and 3 normal Circle of Willis samples from autopsy. The tissue samples were studied with immunohistochemistry.

Results: Although no COX2 expression was found in the normal Circle of Willis, COX2 expression was found in 72% (73/102) of the bAVMs, and localized to the endothelium or luminal surface of bAVM vessels in 48% of the bAVMs. In some bAVM vessels COX2 was also expressed in the medial layer. Interestingly, COX2 expression varied between different vessels of the same bAVM sample. COX2 was expressed by infiltrating inflammatory cells, and correlated with extent of inflammatory cell infiltration (r=0.4, p=0.001). COX2 expression was also found in the brain parenchyme in many cases. COX2 expression did not associate with clinical hemorrhage, nor with histological hemorrhage (hemosiderin) or presence or epilepsy. Association of COX2 expression with molecules mediating vessel remodelling is undergoing.

Conclusion: COX2 expression is induced in many bAVM vessels, as well as in the inflammatory cells that infiltrate the lesion. It seems likely that COX2 signaling participates in the regulation of vessel wall remodelling and inflammation ongoing in the bAVM. The possible role of COX2 signaling as a target for medical therapy stabilizing bAVMs merits further studies, especially since many safe COX2 inhibitors are available in clinical practice.