Journal
NEUROLOGICAL RESEARCH
Volume 29, Issue 4, Pages 356-361Publisher
MANEY PUBLISHING
DOI: 10.1179/016164107X204666
Keywords
traumatic brain injury; heat shock response; cell death
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Funding
- NINDS NIH HHS [R01 NS044100, NS039860] Funding Source: Medline
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Objectives: Our objective was to characterize the heat shock response (HSR) in a model of traumatic brain injury (TBI) and to determine the association of HSR to cell death. Methods: We used immunofluorescent detection of HSP-70 to characterize HSR and TUNEL labeling to determine the pattern of cell death. Results: HSP-70 immunofluorescence revealed a steady increase from 4 to 48 hours following TBI, culminating in a ubiquitous expression with the capillary bed 48 hours post-TBI. TUNEL labeling revealed a small subset of endothelial cell death and a most robust staining of putative pericyte cell death. Discussion: Our results show that while injury causes a detectable stress response, cell death is not a direct consequence of the HSR.
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