An article published this year in “JOURNAL OF CELLULAR AND MOLECULAR
MEDICINE” using our Propidium Iodide (PI)
Solution, by our customers from Department of Physiology, Faculty of Medicine
and Dentistry, University of Valencia, Valencia, Spain, in the study of how
Extracellular histones disarrange vasoactive mediators release through a
COX-NOS interaction in human endothelial cells. Congrats and Thanks.
Summary:
Extracellular histones are
mediators of inflammation, tissue injury and organ dysfunction. Interactions
between circulating histones and vascular endothelial cells are key events in
histone-mediated pathologies. Our aim was to investigate the implication of
extracellular histones in the production of the major vasoactive compounds
released by human endothelial cells (HUVECs), prostanoids and nitric oxide
(NO). HUVEC exposed to increasing concentrations of histones (0.001 to 100
μg/ml) for 4 hrs induced prostacyclin (PGI2) production in a dose-dependent
manner and decreased thromboxane A2 (TXA2) release at 100 μg/ml. Extracellular
histones raised cyclooxygenase-2 (COX-2) and prostacyclin synthase (PGIS) mRNA
and protein expression, decreased COX-1 mRNA levels and did not change
thromboxane A2 synthase (TXAS) expression. Moreover, extracellular histones
decreased both, eNOS expression and NO production in HUVEC. The impaired NO
production was related to COX-2 activity and superoxide production since was
reversed after celecoxib (10 μmol/l) and tempol (100 μmol/l) treatments,
respectively. In conclusion, our findings suggest that extracellular histones
stimulate the release of endothelial-dependent mediators through an up-regulation
in COX-2-PGIS-PGI2 pathway which involves a COX-2-dependent superoxide
production that decreases the activity of eNOS and the NO production. These
effects may contribute to the endothelial cell dysfunction observed in
histone-mediated pathologies.
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