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Hypothermia inhibits human E-selectin transcription
T L Haddix1, T H Pohlman, R F Noel
1Department of Pathology, University of Washington, Seattle, 98195, USA.
The Journal of Surgical Research
|August 1, 1996
Summary
Hypothermia reversibly inhibits E-selectin expression and neutrophil adherence to activated endothelial cells. This effect may explain the protective benefits of hypothermia in clinical settings like cardiopulmonary bypass.
Area of Science:
- Endothelial cell biology
- Immunology
- Molecular biology
Background:
- E-selectin expression on endothelial cells is crucial for neutrophil adhesion during inflammation.
- Transcriptional activation of the E-selectin gene involves transcription factors and cis-acting elements.
Purpose of the Study:
- To investigate the effect of hypothermia on E-selectin expression and neutrophil adherence to activated endothelial cells.
- To determine if hypothermia inhibits E-selectin gene transcription or downstream signaling pathways.
Main Methods:
- Cultured human umbilical vein endothelial cells (HUVECs) were treated with inflammatory stimuli (LPS, IL-1, TNF) at 25°C (hypothermia) or 37°C.
- E-selectin transcript levels, surface expression, and neutrophil adherence were measured.
- NF-kappaB activation was assessed under hypothermic conditions.
Main Results:
- In vitro hypothermia (25°C) transiently inhibited E-selectin gene transcription, surface expression, and neutrophil adherence.
- Rewarming to 37°C restored E-selectin expression and neutrophil adherence to baseline levels.
- Hypothermia did not block NF-kappaB activation, indicating signal transduction remained intact.
Conclusions:
- Neutrophil adherence to activated endothelium mediated by E-selectin is reversibly inhibited by hypothermia.
- The protective clinical effects of hypothermia may be partly due to the transient inhibition of endothelial cell activation phenotypes.