Brain endothelial HSP-70 stress response coincides with endothelial and pericyte death after brain trauma.
OBJECTIVE
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.


CONCLUSIONS
Our results show that while injury causes a detectable stress response, cell death is not a direct consequence of the HSR.
DeGracia
Donald J
DJ
Department of Anatomy and Cell Biology, School of Medicine, Wayne State University, Detroit, MI 48201, USA. jrafols@med.wayne.edu
Kreipke
Christian W
CW
Kayali
Foaz M
FM
Rafols
José A
JA
D000818:Animals; D001921:Brain / Q000378:metabolism*; D001930:Brain Injuries / Q000150:complications / Q000378:metabolism / Q000473:pathology; D016923:Cell Death / Q000502:physiology; D004195:Disease Models, Animal; D004727:Endothelium / Q000378:metabolism* / Q000473:pathology; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism*; D018869:Heat-Shock Response / Q000502:physiology*; D020287:In Situ Nick-End Labeling / Q000379:methods; D008297:Male; D020286:Pericytes / Q000473:pathology / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D018840:HSP70 Heat-Shock Proteins