Hypothermia inhibits human E-selectin transcription. J Surg Res 1996 Aug;64(2):176-83
Date
08/01/1996Pubmed ID
8812630DOI
10.1006/jsre.1996.0325Scopus ID
2-s2.0-0030220098 (requires institutional sign-in at Scopus site) 45 CitationsAbstract
During endothelial cell activation, the formation and expression of E-selectin require transcriptional activation of the E-selectin gene, mediated by the coordinated action of several transcription factors and cis-acting elements in its 5'-flanking region. It is reported that in vitro hypothermia (25 degrees C) transiently inhibits transcriptional activation and surface expression of E-selectin as well as neutrophil adherence to cultured human umbilical vein endothelial cells (HUVECs) treated with lipopolysaccharide (LPS), interleukin-1 (IL-1), or tumor necrosis factor (TNF). Rewarming HUVECs treated with LPS, IL-1, or TNF to 37 degrees C restores E-selectin transcript accumulation, E-selectin surface expression, and neutrophil adherence to HUVECs at levels equivalent to similarly treated HUVECs maintained at 37 degrees C continuously. Despite the absence of detectable E-selectin transcription at 25 degrees C, activation of the transcription factor NF-kappaB still occurred in HUVECs treated with LPS, IL-1, or TNF, indicating that signal transduction was not blocked by hypothermia. It is concluded that neutrophil adherence to activated endothelium mediated by E-selectin is reversibly inhibited by hypothermia. The protective effect of hypothermia clinically (e.g., cardiopulmonary bypass) may, in part, be mediated by transiently inhibiting the expression of an endothelial cell activation phenotype.
Author List
Haddix TL, Pohlman TH, Noel RF, Sato TT, Boyle EM Jr, Verrier EDMESH terms used to index this publication - Major topics in bold
Antibodies, MonoclonalBase Sequence
Cold Temperature
E-Selectin
Endothelium, Vascular
Enzyme-Linked Immunosorbent Assay
HL-60 Cells
Hot Temperature
Humans
Hypothermia
Interleukin-1
Lipopolysaccharides
Molecular Sequence Data
Phenotype
RNA, Messenger
Signal Transduction
Transcription, Genetic
Tumor Necrosis Factor-alpha
Umbilical Veins
