Biological response of human aortic endothelial cells exposed to acellular hemoglobin solutions developed as potential blood substitutes

Marie Toussaint-Hacquard*, Y. Devaux, D. Longrois, B. Faivre-Fiorina, S. Muller, J. F. Stoltz, C. Vigneron, P. Menu

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

11 Citations (Scopus)

Abstract

The cardiovascular effects of hemoglobin-based oxygen carriers (HBOCs) are mainly related to their nitric oxide (NO) scavenging properties but other effects such as the impact of these hemoglobins on the endothelial cell (EC) biology are not well understood. We hypothesized that HBOCs could modify EC functions by altering gene expression, in particular the endothelial NO synthase (NOS3) and/or by activating EC. Cultured human aortic endothelial cells (HAEC) were incubated for 3 hours with purified cell-free Hb, Dex-BTC-Hb or αα-Hb (16 g/L). Expression of NOS3 mRNA and protein were assessed by semi-quantitative RT-PCR and Western blot respectively immediately after and 24 hours after incubation. The expression and localization of the adhesion molecule ICAM-1 were detected by fluorescence microscopy. None of the solutions tested modified NOS3 mRNA and protein expression despite adequate controls that up- or down-regulate NOS3 expression. The expression and the localization of ICAM-1 on the cell membrane were modified after 3 hours of incubation with all the hemoglobin solutions tested in a manner similar to tumor necrosis factor-α. In conclusion, HAEC incubation with clinically relevant concentrations of HBOCs induced changes in the pattern of ICAM-1 expression consistent with cell activation/cell signaling mechanisms. However, HBOCs did not alter NOS3 gene expression.

Original languageEnglish
Pages (from-to)1143-1157
Number of pages15
JournalLife Sciences
Volume72
Issue number10
DOIs
Publication statusPublished - 24 Jan 2003
Externally publishedYes

Keywords

  • Blood substitute
  • Cell-free hemoglobin
  • Endothelial cell
  • ICAM-1
  • Nitric oxide synthase

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