Cell-specific DNA fragmentation may be attenuated by a survivin-dependent mechanism after traumatic brain injury in rats

Erik A. Johnson, Stanislav I. Svetlov, Kevin K.W. Wang, Ronald L. Hayes, Jose A. Pineda

Research output: Contribution to journalArticle

27 Scopus citations

Abstract

Survivin attenuates apoptosis by inhibiting cleavage of some cell proteins by activated caspase-3. We recently discovered strong up-regulation of survivin, primarily in astrocytes and a sub-set of neurons, after traumatic brain injury (TBI) in rats. In this study we characterized co-expression of survivin with activated caspase-3 and downstream DNA fragmentation (TUNEL) in astrocytes and neurons after TBI. Western blot analysis revealed significant time-dependent increases in active caspase-3 between 5 and 14 days post-injury. No difference was observed between the proportion of survivin-positive and survivin-negative cells labeled with active caspase-3 at 5 or 7 days post-injury, as indicated by dual fluorescent immunostaining. Labeling of survivin-negative cells with TUNEL was, however, significantly greater than for survivin-positive cells, suggesting that expression of survivin may attenuate DNA cleavage and progression of apoptosis. A higher proportion of astrocytes than neurons accumulated active caspase-3. In contrast, co-localization with TUNEL was significantly higher for neurons than for astrocytes. These data suggest that survivin expression may attenuate DNA cleavage and cell death, and that this mechanism operates in a cell type-specific manner after TBI.

Original languageEnglish
Pages (from-to)17-26
Number of pages10
JournalExperimental Brain Research
Volume167
Issue number1
DOIs
StatePublished - Nov 1 2005

Keywords

  • Astrocyte
  • Caspase-3
  • Inhibitor of apoptosis protein
  • Neuron
  • Survivin
  • Traumatic brain injury

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