Abstract
Objectives
Preeclampsia (PE) occurs as a result placental hypoxia-induced oxidative and endoplasmic
reticulum stress, and is associated with the activation of hypoxia inducible factor-1α
(HIF-1α) and apoptotic CHOP pathways with the consequential shedding of syncytiotrophoblast
microvesicles which may be central in mediating the maternal systemic immune response.
The aim of this study was to immune-localise and morphometrically analyse CHOP and
HIF-1α within the placenta of normotensive and pre-eclamptic pregnancies and concomitantly
quantify syncytiotrophoblast released microvesicles in maternal circulation.
Study design
Placental tissue and plasma were obtained from normotensive and pre-eclamptic pregnant
women. The expression of CHOP and HIF-1α was analysed using immunohistochemistry.
Isolation and size distribution of the circulating maternal microvesicles was determined
using nanoparticle tracking analysis. The concentration of syncytiotrophoblast microvesicles
was determined using the placental alkaline phosphatase ELISA.
Results
This study demonstrates a significant increase in immunohistochemical expression of
HIF-1 α and CHOP in preeclampsia compared to the normotensive women (p < 0.05). In keeping with this, a significant increase in the mean syncytiotrophoblast
microvesicles concentration was observed in PE, compared to normotensives (p < 0.05). A positive correlation between placental expression of CHOP and HIF-1α and
STBMs was obtained.
Conclusion
This study demonstrates increased placental expression of HIF-1α and CHOP in preeclampsia
compared to normotensive pregnancies which correlate to their increased syncytiotrophoblast
microvesicles concentration in maternal circulation. These findings indicate that
placental hypoxia and ER stress are interrelated contributory factors to the pathogenesis
of PE and the consequential release of placental derived debris into the maternal
circulation.
Keywords
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Article info
Publication history
Published online: November 07, 2017
Accepted:
November 6,
2017
Received in revised form:
November 3,
2017
Received:
May 15,
2017
Identification
Copyright
© 2017 Elsevier B.V. All rights reserved.
