Sera from early-onset, severely preeclamptic women directly modulate HLA-E expression in the EA.hy296 endothelial cell line.
The expression of endothelial HLA-E in the context of the systemic inflammatory response observed in preeclampsia has not been established. An experimental study was designed to determine the effect of the sera of pregnant women on the expression of HLA-E in EA.hy296 endothelial cells. First, measurements of protein fractions were performed in sera from early-onset, severely preeclamptic women without HELLP syndrome, in which there was no significant difference in total proteins between the groups, but a reduced level of plasma albumin and an increase in α1-globulin were observed in both groups of pregnant women compared with non-pregnant women. Measurements of colloid osmotic pressure (COP) using a recalculated albumin/globulin ratio formula determined only a significant decrease in COP in all pregnant groups compared with non-pregnant women. The expression of membrane HLA-E was increased in EA.hy296 endothelial cells stimulated with sera of early-onset, severely preeclamptic women, while recombinant interferon-γ (IFN-γ) significantly reduced the expression of membrane HLA-E. Pro-inflammatory cytokines were measured by Luminex in the serum samples, and increased levels of tumor necrosis factor (TNF) and decreased levels of IFN-γ were observed in early-onset, severe preeclampsia compared with normal pregnancy. Moreover, soluble HLA-E was detected in these serum samples by Western blot and ELISA, but no significant difference was found. This raises the possibility that a systemic inflammatory response promotes a compensatory mechanism of COP balance in severe preeclampsia by release of inflammation-induced factors, including endothelial HLA-E. Evidence is now provided regarding HLA-E expression by EA.hy296 cells.
Reproduction Group, Universidad de Antioquia, Calle 70 No. 52-21, Medellin, Colombia; Department of Physiology and Biochemistry, Universidad de Antioquia, Calle 70 No. 52-21, Medellin, Colombia. Electronic address: julio.bueno@udea.edu.co.
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Bueno-Sánchez
Reproduction Group, Universidad de Antioquia, Calle 70 No. 52-21, Medellin, Colombia.
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Peña-Alzate
Reproduction Group, Universidad de Antioquia, Calle 70 No. 52-21, Medellin, Colombia.
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Peña
NACER-SSR, Department of Obstetrics and Gynaecology, School of Medicine, Universidad de Antioquia, Calle 70 No. 52-21, Medellin, Colombia; Hospital Universitario San Vicente Fundación and Hospital General de Medellín, Obstetrics and Gynaecology Services, Medellín, Colombia.
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Agudelo-Jaramillo
Reproduction Group, Universidad de Antioquia, Calle 70 No. 52-21, Medellin, Colombia.
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Cadavid-Jaramillo
INSERM U 976, Pavillon Bazin, Hopital Saint Louis, 75010 Paris, France.
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Chaouat
Reproduction Group, Universidad de Antioquia, Calle 70 No. 52-21, Medellin, Colombia; Centauro Group, School of Veterinary Medicine, Universidad de Antioquia, Calle 70 No. 52-21, Medellin, Colombia.
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Maldonado-Estrada
D045744:Cell Line, Tumor; D042783:Endothelial Cells / Q000276:immunology / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects* / Q000276:immunology; D015395:Histocompatibility Antigens Class I / Q000096:biosynthesis* / Q000276:immunology; D006801:Humans; D007371:Interferon-gamma / Q000097:blood / Q000276:immunology; D011225:Pre-Eclampsia / Q000097:blood* / Q000276:immunology; D011247:Pregnancy; D011446:Prospective Studies; D044967:Serum; D012720:Severity of Illness Index; D000097625:HLA-E Antigens
D015395:Histocompatibility Antigens Class I; D007371:Interferon-gamma; D000097625:HLA-E Antigens; C573415:IFNG protein, human
Early-onset severe preeclampsia; Endothelial cells.; HLA-E; Systemic inflammatory response syndrome