gms | German Medical Science

64th Annual Meeting of the German Society of Neurosurgery (DGNC)

German Society of Neurosurgery (DGNC)

26 - 29 May 2013, Düsseldorf

InterCellularAdhesionMolecule-1 (ICAM1) and P-SelectinGlycoproteinLigand-1 (PSGL1) contribute to neuronal apoptosis after experimental subarachnoid haemorrhage via endovascular inflammatory processes

Meeting Abstract

  • Etienne N. Atangana - Neurochirurgische Klinik, Charité – Universitätsmedizin Berlin
  • Ulf C. Schneider - Neurochirurgische Klinik, Charité – Universitätsmedizin Berlin
  • Salima Magrini - Neurochirurgische Klinik, Charité – Universitätsmedizin Berlin
  • Peter Vajkoczy - Neurochirurgische Klinik, Charité – Universitätsmedizin Berlin

Deutsche Gesellschaft für Neurochirurgie. 64. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Düsseldorf, 26.-29.05.2013. Düsseldorf: German Medical Science GMS Publishing House; 2013. DocMO.09.01

doi: 10.3205/13dgnc071, urn:nbn:de:0183-13dgnc0710

Published: May 21, 2013

© 2013 Atangana et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Objective: Inflammatory mechanisms have become an interesting target for early and delayed brain injury after subarachnoid hemorrhage (SAH). Our group could demonstrate an intravascular leukocyte activation, which preceeded an intraparenchymal microglia activation in the central nervous system (CNS) after SAH. This endovascular inflammatory reaction peaks 2-4 days after the bleeding. To evaluate if the depletion of leukocyte endothelial interaction would attenuate secondary brain injury, mouse knockout models were applied.

Method: Experimental SAH was induced in ICAM- and PSGL-knockout mice through endovascular perforation. Leukocyte endothelial interaction was quantified using the chronic cranial window technique. Wildtype mice and sham operated animals served as controls. Neuronal injury was evaluated in frozen brain sections using a NeuN/TUNEL Kit co-staining and counting of apoptoses in serial sections.

Results: A marked increase of neuronal apoptosis was documented on day 7 and 14 after SAH in wildtype animals compared to sham animals (day7: 212 ± 125 vs. 98 ± 19; day14: 273 ± 127 vs. 63 ± 21 (apoptosis counts per brain slice)). Increased rolling and sticking activity of leukocytes was documented in SAH animals. In ICAM knockout mice, the sticking activity was significantly impaired, in PSGL knockout mice, rolling and sticking activity were significantly impaired after SAH between days 2 and 4. The neuronal apoptosis was markedly reduced in both, PSGL- and ICAM-knockout mice on days 7 and 14, compared to wildtype animals. Yet, a significance (p < .05) could only be documented in ICAM knockout mice (day7: 47 ± 7; 169 ± 28 day14: 76 ± 8; 152 ± 29 (ICAM;PSGL; apoptosis counts per brain slice)).

Conclusions: Intravascular leukocyte endothelial interaction precedes a neuronal loss after subarachnoid hemorrhage. Depletion of the two major ligands leads to a significant reduction of neuronal apoptosis. These results promote our theory of an inflammatory cascade as possible cause of secondary brain injury after SAH.