gms | German Medical Science

55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

25. bis 28.04.2004, Köln

S100B protein reduces delayed neuronal injury in stretch injured mixed glial-neuronal cell cultures

S100B-Protein reduziert die protrahierte neuronale Dysfunktion nach stretch injury von gemischt neuronal-glialen Zellkulturen

Meeting Abstract

  • corresponding author Andrea Kleindienst - Department of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond /USA
  • K. A. Willoughby - Department of Pharmacology, Medical College of Virginia, Virginia Commonwealth University, Richmond /USA
  • C. Mueller - Institute of Laboratory Medicine and Pathobiochemistry Charité, Humboldt University Berlin, Berlin
  • E. F. Ellis - Department of Pharmacology, Medical College of Virginia, Virginia Commonwealth University, Richmond /USA

Deutsche Gesellschaft für Neurochirurgie. Ungarische Gesellschaft für Neurochirurgie. 55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie. Köln, 25.-28.04.2004. Düsseldorf, Köln: German Medical Science; 2004. DocP 02.17

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2004/04dgnc0300.shtml

Veröffentlicht: 23. April 2004

© 2004 Kleindienst et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective

S100B protein has been localized primarily to astrocytes and is increased in astrocytes and in extracellular fluid after in vitro or in vivo brain trauma or ischemia. Experimental evidence has suggested that S100B release following injury may serve in a paracrine function to reduce neuronal injury or promote neuronal recovery. We examined whether S100B alters the response of neuronal plus glial cell cultures to strain (stretch) injury.

Methods

Following injury, astrocyte nuclei normally take up the dye propidium iodide (PrI) at 15 minutes after injury but by 24 and 48 hr the astrocytes repair and regain their capacity to exclude PrI. In an opposite manner, stretch injured neurons do not take up PrI until approximately 24-48 hr after injury. We examined the spontaneous release of S100B, and the effect of S100B (10 or 100 nM) added at different time points on the PrI uptake of astrocytes and neurons for 48hr after stretch injury.

Results

The spontaneous S100B release started immediately after injury and incresed up to 60ng/l at 48hr. In neurons, 10 or 100 nM S100B given at 6hr and at 24 hr after injury reduced PrI uptake at 48 hr by 30% (p < 0.05). S100B given 15 min before or within 5 sec of injury had no consistent effect on astrocyte PrI uptake at 15 min after injury.

Conclusions

These results support a possible protective or recovery-enhancing role for S100B in neurons following injury. Thereby, post -traumatic release of S100B by astrocytes may contribute to endogenous repair mechanisms.