gms | German Medical Science

57th Annual Meeting of the German Society of Neurosurgery
Joint Meeting with the Japanese Neurosurgical Society

German Society of Neurosurgery (DGNC)

11 - 14 May, Essen

Matrix metalloproteinases (MMP)-9 and 2 might play a Janus-headed role for the development of cerebral edema following SAH

Mögliche Janus-köpfige Bedeutung der Matrix Metalloproteinasen (MMP)-9 und 2 für die Entwicklung des Hirnödems nach SAB

Meeting Abstract

  • corresponding author K. Schöller - Neurochirurgische Klinik, Klinikum der Universität München-Großhadern
  • A. Trinkl - Neurologische Klinik, Klinikum der Universität München-Großhadern
  • M. Klopotowski - Institut für Chirurgische Forschung, Klinikum der Universität München-Großhadern
  • N. Plesnila - Institut für Chirurgische Forschung, Klinikum der Universität München-Großhadern
  • R. Schmid-Elsaesser - Neurochirurgische Klinik, Klinikum der Universität München-Großhadern
  • S. Zausinger - Neurochirurgische Klinik, Klinikum der Universität München-Großhadern

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 57. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie. Essen, 11.-14.05.2006. Düsseldorf, Köln: German Medical Science; 2006. DocP 10.150

The electronic version of this article is the complete one and can be found online at:

Published: May 8, 2006

© 2006 Schöller 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: Mechanisms of early cerebral edema following subarachnoid hemorrhage (SAH) are poorly understood. Matrix metalloproteinases (MMP)-9 and 2 are known to degrade microvascular basal lamina proteins in focal cerebral ischemia and might therefore also contribute to blood-brain barrier (BBB) damage and the formation of vasogenic cerebral edema after SAH.

Methods: Rats were subjected to SAH using the endovascular puncture method and assigned to groups with different survival (6, 24, 48, and 72 hours after SAH, respectively). MMP expressions were measured by gelatin zymography in the cerebral cortex and subcortical regions. Microvascular basal lamina alteration was quantified by collagen type IV immunochemistry, BBB permeability was assessed by Bovine serum albumin Western Blot.

Results: BBB disruption, basal lamina damage, and MMP-9 expression occurred to the most extent in the ipsilateral cortex. Furthermore, the time course of BBB damage is paralleled by the expression of MMP-9 starting at 6 hours and peaking at 48 hours after SAH. MMP-9 expression correlates significantly with basal lamina damage (R=-0.53; P=0.004), and with BBB permeability (R=0.47; P=0.01). In contrast to MMP-9, primarily subcortical MMP-2 expression is less pronounced, not detectable until 24 hours and increasing until 72 hours after SAH.

Conclusions: MMP-9 might contribute to the development of vasogenic brain edema following SAH by digesting microvascular basal lamina collagen IV leading to BBB permeability. MMP-2 expression after SAH has not been investigated before. The relatively late and primarily subcortical expression could be a protective mechanism to promote neuronal plasticity. Further investigations with pharmacological MMP inhibition or genetic knock-out experiments need to be carried out to further elucidate the role of the MMP system as a potential target for therapeutic interventions to prevent development of cerebral edema following SAH.