gms | German Medical Science

68th Annual Meeting of the German Society of Neurosurgery (DGNC)
7th Joint Meeting with the British Neurosurgical Society (SBNS)

German Society of Neurosurgery (DGNC)

14 - 17 May 2017, Magdeburg

PLOD2 expression in brain arteriovenous malformations (bAVM) and ist association with bAVM size

Meeting Abstract

  • Belal Neyazi - Klinik für Neurochirurgie, KRH Klinikum Nordstadt, Hannover, Hannover, Deutschland
  • Levent Tanrikulu - Klinik für Neurochirurgie, KRH Klinikum Nordstadt, Hannover, Hannover, Deutschland
  • Klaus-Peter Stein - Klinik für Neurochirurgie, KRH Klinikum Nordstadt, Hannover, Hannover, Deutschland
  • Claudia A. Dumitru - Klinik für Neurochirurgie, KRH Klinikum Nordstadt, Hannover, Hannover, Deutschland
  • I. Erol Sandalcioglu - Klinik für Neurochirurgie, KRH Klinikum Nordstadt, Hannover, Hannover, Deutschland

Deutsche Gesellschaft für Neurochirurgie. Society of British Neurological Surgeons. 68. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 7. Joint Meeting mit der Society of British Neurological Surgeons (SBNS). Magdeburg, 14.-17.05.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocMO.02.06

doi: 10.3205/17dgnc012, urn:nbn:de:0183-17dgnc0123

Published: June 9, 2017

© 2017 Neyazi 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: Brain arteriovenous malformations (bAVM) are severe conditions which, upon rupture, cause debilitating neurological deficits and even death. The exact cellular/ molecular mechanisms associated with bAVM growth and rupture are currently unclear. The objective of this study was to explore the potential role of PLOD2 (Procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2) in bAVM pathophysiology.

Methods: Expression and localization of PLOD2 were assessed immunohistochemically in tissue microarrays from bAVM patients (n=60). Correlations between PLOD2 levels and clinical parameters were assessed with Pearson's test or Spearman’s rank correlation coefficient. Comparison between different clinical parameters was performed using t-test or non-parametric Mann-Whitney U-test. Fisher's exact test was used for categorical data.

Results: PLOD2 was mainly expressed within the tunica media of blood vessels. High levels of PLOD2 expression correlated with small bAVM size (p=0.0083, R²=0.158). Small bAVM showed an increased frequency of hemorrhage compared to large ones (p=0.001). Although PLOD2 was not directly associated with bAVM hemorrhage, high PLOD2-expressing bAVM had a lower frequency of hemorrhage compared to low or medium PLOD2-expressing bAVM (25% versus 63% and 75%, respectively).

Conclusion: Our study reports for the first time that PLOD2 is expressed in bAVM and suggests a role of PLOD2 in bAVM pathophysiology. These findings contribute to a better understanding of the bAVM microenvironment and may foster the development of improved therapeutic strategies against this disease.