Endothelial monocyte-activating polypeptide-2 is increased in pregnancy but is not further increased in preeclampsia

Endothelial monocyte-activating polypeptide-2 (EMAP-2) is a novel protein that demonstrates potent proinflammatory activity in vivo and in vitro. The purpose of this study was to investigate the expression of EMAP-2 in normal pregnancy and in pregnancies complicated with preeclampsia and to test the...

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Veröffentlicht in:Journal of the Society for Gynecologic Investigation 1999-05, Vol.6 (3), p.142-146
Hauptverfasser: WELLINGS, R. P, LASH, G. E, MURRAY, J. C, TAS, M, WARD, W, TREW, A. J, BAKER, P. N
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Sprache:eng
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Zusammenfassung:Endothelial monocyte-activating polypeptide-2 (EMAP-2) is a novel protein that demonstrates potent proinflammatory activity in vivo and in vitro. The purpose of this study was to investigate the expression of EMAP-2 in normal pregnancy and in pregnancies complicated with preeclampsia and to test the hypothesis that EMAP-2 is a causative agent of the endothelial activation of preeclampsia. Expression of EMAP-2 in the placenta was investigated using reverse transcriptase-polymerase chain reaction to detect mRNA, and immunohistochemistry with an EMAP-2-specific polyclonal antiserum was carried out to detect protein. Levels of circulating EMAP-2 protein were measured in the blood of nonpregnant, normal pregnant, and preeclamptic individuals using a specific enzyme-linked immunoabsorbent assay and the molecular forms present assessed by Western blotting. EMAP-2 is transcribed and translated by the placenta troughout pregnancy and in preeclampsia and can be detected in the plasma of nonpregnant and pregnant individuals. Levels of circulating EMAP-2 antigen are raised in pregnancy compared with nonpregnant controls; however, levels in patients with preeclampsia are identical to those in normal pregnant individuals. While circulating levels of EMAP-2 are increased in pregnancy, there is no evidence that EMAP-2 is involved directly in the pathogenesis of preeclampsia.
ISSN:1071-5576
1556-7117
DOI:10.1016/S1071-5576(99)00011-8