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.
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.